Pemphigus represents a group of potentially life-threatening autoimmune blistering diseases characterized by the production of pathogenic autoantibodies against desmosomal cadherins, leading to loss of cell adhesion. Early and accurate diagnosis remains critical for optimal management, yet current diagnostic approaches largely rely on invasive biopsies and serological assays that do not always predict disease progression or therapeutic response. In this context, the identification of reliable biomarkers is essential to enhance diagnostic precision, monitor disease activity, and guide treatment strategies. Non-coding RNAs (ncRNAs), particularly microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), have emerged as promising biomarker candidates due to their stability in body fluids, tissue- and disease-specific expression patterns, and regulatory functions in immune processes. Increasing evidence suggests that dysregulated ncRNAs play significant roles in the immunopathogenesis of pemphigus, influencing cytokine signaling, immune cell differentiation, and keratinocyte adhesion. Therefore, herein, we summarize current findings on the involvement of specific miRNAs and lncRNAs in pemphigus pathogenesis, their diagnostic and prognostic potential, and the emerging therapeutic opportunities based on modulating ncRNA expression. Additionally, we address the limitations and challenges associated with clinical translation of ncRNA research and highlight future directions that may facilitate the incorporation of ncRNAs into personalized medicine approaches for pemphigus patients.

Hypertension is a prevalent disease that substantially elevates the risk of neurological disorders such as dementia, stroke and Parkinson's disease. MicroRNAs (miRNAs) play a critical role in the regulation of gene expression related to brain function and disorders. Understanding the involvement of miRNAs in these conditions could provide new insights into potential therapeutic targets. The main objective of this study is to target and investigate microRNAs (miRNAs) associated with neurological disorders in patients suffering from hypertension. The genes involved in hypertension were identified from various databases including GeneCard, MalaCard, DisGeNet, OMIM & GEO2R. The key gene for hypertension was identified using a systems biology approach. Also, potent phytochemical for hypertension was determined by computer-aided drug-designing approach. Functional miRNAs were determined for the key target gene using miRNet analytics platform by hypergeometric tests. Further, the gene-miRNA interaction was determined and enrichment analysis was done. RPS27A was identified as a key target gene for hypertension. Naringenin showed effective molecular interaction with RPS27A with a binding energy score (-6.28). Further, a list of miRNAs which were targeting brain disorders was determined from miRNet. A gene-miRNA network was constructed using the PSRR tool for Parkinson's Disease, Autism Spectrum Disorder, Acute Cerebral Infarction, ACTH-Secreting Pituitary Adenoma, & Ependymoma. Further, miRNA 21 & miRNA 16 were found to be associated with four of the neurological disorders. The study identifies specific miRNAs that may serve as potential biomarkers for brain disorders in hypertensive patients. Targeting these miRNAs could open new avenues for therapeutic strategies aimed at mitigating neurological damage in this patient population.

Venezuelan equine encephalitis virus (VEEV) is an alphavirus in the family Togaviridae, transmitted by a mosquito bite and is highly infectious in aerosol form. Inflammation plays a role of antiviral response as well as development of lethal encephalitis. Infection through a mosquito bite is biphasic, beginning with an inflammatory process and viral replication in different organs with subsequent infiltration to the central nervous system (CNS), inducing encephalitis. The direct route is through inhalation of aerosols containing the virus with direct brain infection through the olfactory nerve. Significant damage is due to exacerbated inflammation in the host. Angiotensin II (Ang II) is a molecule with high pro-inflammatory capacity, which has been found to be upregulated in the brain of VEEV-infected rats, suggesting its role in the pathogenesis of this disease. Limited information regarding the association of Ang II expression with VEEV brain infection has been reported. The aim of this review is to highlight published reports indicating a possible association between Ang II expression and VEEV-induced encephalitis. Several studies reflect a possible expression and function of Ang II during VEEV infection. Factors such as the relationship of Ang II with proteins involved in viral replication and entry into the cell (furin, Rab5, Rab7), activation of protein kinase C (necessary for the phosphorylation of VEEV), presence of microRNAs related to viral biology, increased permeability of the blood-brain barrier, and use of transcription pathways common to Ang II and VEEV, may conceivable an association of Ang II with the pathogenesis of VEEV encephalitis.

miR-19-3p has been implicated in various pathological and physiological processes, including immune response, inflammation, oncogenesis and cell damage. However, its function in rainbow trout (Oncorhynchus mykiss) has not been well elucidated. In this study, the expression patterns of miR-19-3p and target gene DExH-Box helicase 58 (DHX58) in rainbow trout infected with infectious hematopoietic necrosis virus (IHNV) were detected, and regulatory mechanism and function of miR-19-3p were investigated by overexpression and inhibition experiment in vitro and in vivo. Expression patterns showed that miR-19-3p and DHX58 displayed significant time-dependent changes in IHNV-infected rainbow trout intestines, skins, gills, and liver cells, and their expression were negatively correlated at multiple time points. In vitro, the targeting relationship between miR-19-3p and DHX58 was confirmed by dual-luciferase reporter assay and RNA immunoprecipitation assay, and overexpression of miR-19-3p significantly suppressed the expression of DHX58 and downstream genes interferon regulatory factor 3 (IRF3), interferon regulatory factor 7 (IRF7), interferon (IFN), myxovirus 1 (MX1), interferon-stimulated gene 15 (ISG15), nuclear factor kappa-B (NF-κB), and interleukin-1 beta (IL-1β), whereas the expression levels of DHX58 and downstream genes were significantly increased after transfecting miR-19-3p inhibitor. In vivo, agomiR-19-3p significantly inhibited the expression of DHX58, and then reduced the expression levels of IRF3, IRF7, IFN, MX1, NF-κB, IL-1β, tumor necrosis factor-α (TNFα), and ISG15. Additionally, overexpression of miR-19-3p significantly increased IHNV copies and cell proliferation number, and suppressed apoptosis, while the opposite results were obtained after miR-19-3p repressing. This study confirmed that miR-19-3p regulates rainbow trout antiviral immune by DHX58-mediated interferon pathway in vitro and in vivo, which provides potential for using miRNAs as anti-viral target drugs.

Millions of people worldwide, especially young adults, are affected by multiple sclerosis (MS), a demyelinating and autoimmune condition of the central nervous system (CNS). Many studies have focused on the diagnostic value of miRNAs circulating in body fluids of MS patients. Thus, this study aimed to assess the expression of miR-128 and its potential as a biomarker for MS in the Iranian population.

This study recruited 85 MS patients and 30 healthy matched controls. Following the collection of blood samples, serum was isolated. RNA was then extracted, cDNA was synthesized, and miR-128 expression was measured by real-time PCR.

There was significant overexpression of miR-128 in MS patients in comparison with healthy controls (p-value <0.0001). In addition, there was a rather notable association between the subtypes of MS samples and the expression levels of miR-128. ROC analysis showed an AUC of 0.9111 (95%CI 0.85-0.97, p-value <0.0001) with sensitivity and specificity of 80.00% and 93.33%, respectively.

The expression of miR-128 was significantly higher in PBMCs of MS patients in comparison with healthy controls. Additionally, miR-128 could be an excellent biomarker for MS patient diagnosis.

Traditional microRNA detection methods have some limitations that cannot be ignored. Enzyme-catalyzed nucleic acid amplification has gradually become an important method in bioanalysis and is expected to be a substitute for traditional methods. Combining enzymes with different functions provides a wide range of analytical design possibilities to create high-performance sensing strategies. Meanwhile, the optical tweezers that produce the tightly focused laser beam are integrated with a suspension bead array that fully concentrates the signal labels, contributing to stable signal output and improved detection efficiency. Herein, we have developed a novel "DSN-RCA dual amplification and optical tweezer-assisted suspension bead array imaging" sensing strategy for highly efficient detection of microRNA-21 (miRNA-21). The conversion of low abundance targets into bulk fluorescence signal probes was achieved by duplex-specific nuclease (DSN), and signal enrichment on bead supports rather than dispersion in solution was realized by rolling circle amplification (RCA) in one step. The synergistic integration of dual amplification and the application of bead supports effectively improved the sensitivity and specificity. Finally, the suspension bead array was created by the modified optical tweezer system, which realized the high-quality imaging analysis and improved the detection efficiency. The proposed sensing strategy achieved a limit of detection (LOD) as low as 5.90 pM with excellent specificity, stability, and reproducibility and was successfully applied to human serum samples, which has great potential for application in clinical serological research.

Sepsis is a highly dangerous and complex condition that can result in death. It is characterized by a strong reaction to an infection, causing dysfunction in multiple bodily systems and a high risk of mortality. The transformation of macrophages is a vital stage in the procedure as they possess the capability to interchange between two separate types: M1, which promotes inflammation, and M2, which inhibits inflammation. The choice greatly affects the immune response of the host. This analysis underscores the rapidly expanding roles of exosomes and microRNAs (miRNAs) in regulating the trajectory of macrophage polarization during episodes of sepsis. Exosomes, extremely small extracellular vesicles, facilitate cellular communication by transferring biologically active compounds, including miRNAs, proteins, and lipids. We investigate the impact of changes in exosome production and composition caused by sepsis on macrophage polarization and function. Unique microRNAs present in exosomes play a significant role in controlling crucial signaling pathways that govern the phenotype of macrophages. Through thorough examination of recent progress in this area, we clarify the ways in which miRNAs derived from exosomes can either aggravate or alleviate the inflammatory reactions that occur during sepsis. This revelation not only deepens our comprehension of the underlying mechanisms of sepsis, but it also reveals potential new biomarkers and targets for treatment. This assessment aims to amalgamate diverse research investigations and propose potential avenues for future investigations on the influence that exosomes and miRNAs have on macrophage polarization and the body's response to sepsis. These entities are essential for controlling the host's reaction to sepsis and hold important functions in this mechanism.

In plants and animals, the microRNA (miRNA) class of small regulatory RNA plays an essential role in controlling gene expression in all aspects of development, to respond to environmental stress, or to defend against pathogen attack. This well-established master regulatory role for miRNAs has led to each protein-mediated step of both the plant and animal miRNA pathways being thoroughly characterized. Furthermore, this degree of characterization has led to the development of a suite of miRNA-based technologies for gene expression manipulation for fundamental research or for use in industrial or medical applications. In direct contrast, molecular research on the miRNA pathway of macroalgae, specifically seaweeds (marine macroalgae), remains in its infancy. However, the molecular research conducted to date on the seaweed miRNA pathway has shown that it shares functional features specific to either the plant or animal miRNA pathway. In addition, of the small number of seaweed species where miRNA data is available, little sequence conservation of individual miRNAs exists. These preliminary findings show the pressing need for substantive research into the seaweed miRNA pathway to advance our current understanding of this essential gene expression regulatory process. Such research will also generate the knowledge required to develop novel miRNA-based technologies for use in seaweeds. In this review, we compare and contrast the seaweed miRNA pathway to those well-characterized pathways of plants and animals and outline the low degree of miRNA sequence conservation across the polyphyletic group known as the seaweeds.

Our previous research indicated that Sodium houttuyfonate (SH) can effectively ameliorate dextran sulfate sodium (DSS)-induced colitis exacerbated by Candida albicans. However, the underlying protective mechanism of SH remains unclear. Therefore, in this study, a mice colitis model was infected with C. albicans, and the total colonic miRNAs were assessed. Furthermore, the differentially expressed miRNAs were enriched, clustered, and analyzed. Moreover, based on the dual luciferase analysis of NFKBIZ modulation by miR-32-5p, the in vitro and in vivo therapeutic effects of SH on inflammatory response, fungal burden, oxidative stress, and apoptosis were assessed at transcriptional and translational levels in the presence of agonist and antagonist. A total of 1157 miRNAs were identified, 84 of which were differentially expressed. Furthermore, qRT-PCR validated that SH treatment improved 17 differentially expressed miRNAs with > fourfold upregulation or > sixfold downregulation. Similar to most differentially altered miRNA, C. albicans significantly increased Dectin-1, NF-κB, TNF-α, IL-1β, IL-17A, and decreased miR-32-5p which negatively targeted NFKBIZ. In addition, SH treatment reduced inflammatory response and fungal burden in a colitis model with C. albicans infection. Further analyses indicated that in C. albicans infected Caco2 cells, SH inhibited fungal growth, oxidative stress, and apoptosis by increasing Dectin-1, NF-κB, NFKBIZ, TNF-α, IL-1β, IL-17A, and decreasing miR-32-5p. Therefore, SH can ameliorate the severity of colitis aggravated by C. albicans via the Dectin-1/NF-κB/miR-32-5p/NFKBIZ axis.

MicroRNAs (miRNAs) are classified as small, non-coding RNAs that play crucial roles in diverse biological processes, including cellular development, differentiation, growth, and metabolism. MiRNAs regulate gene expression by recognizing complementary sequences within messenger RNA (mRNA) molecules. Recent studies have revealed that miR-145-5p functions as a tumor suppressor in several cancers, including lung, liver, and breast cancers. Notably, miR-145-5p plays a vital role in the pathophysiology underlying HIV and chronic obstructive pulmonary diseases associated with cigarette smoke. This miRNA is abundant in biofluids and shows potential as a biomarker for the diagnosis and prognosis of several infectious diseases, such as hepatitis B, tuberculosis, and influenza. Additionally, numerous studies have indicated that other non-coding RNAs, including long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs), can regulate miR-145-5p. Given the significance of miR-145-5p, a comprehensive overview focusing on its roles in health and disease is essential. This review discusses the dual role of miR-145-5p as a protagonist and antagonist in important human diseases, with particular emphasis on disorders of the respiratory, digestive, nervous, reproductive, endocrine, and urinary systems.

Cancer is a rising issue worldwide, and numerous studies have focused on understanding the underlying reasons for its occurrence and finding proper ways to defeat it. By applying technological advances, researchers are continuously uncovering and updating treatments in cancer therapy. Their vast functions in the regulation of cell growth and proliferation and their significant role in the progression of diseases, including cancer. This review provides a comprehensive analysis of ncRNAs in breast cancer, focusing on long non-coding RNAs such as HOTAIR, MALAT1, and NEAT1, as well as microRNAs such as miR-21, miR-221/222, and miR-155. These ncRNAs are pivotal in regulating cell proliferation, metastasis, drug resistance, and apoptosis. Additionally, we discuss experimental approaches that are useful for studying them and highlight the advantages and challenges of each method. We then explain the results of these clinical trials and offer insights for future studies by discussing major existing gaps. On the basis of an extensive number of studies, this review provides valuable insights into the potential of ncRNAs in cancer therapy. Key findings show that even though the functions of ncRNAs are vast and undeniable in cancer, there are still complications associated with their therapeutic use. Moreover, there is an absence of sufficient experiments regarding their application in mouse models, which is an area to work on. By emphasizing the crucial role of ncRNAs, this review underscores the need for innovative approaches and further studies to explore their potential in cancer therapy.

HIV-1 infection induces persistent immune system activation despite antiretroviral therapy. New immunomodulatory targets might be required to restore immune competence. The dendritic cells immunoreceptor (DCIR) can bind HIV-1 and regulate immune functions and extracellular vesicles (EVs) production. EVs have emerged as biomarkers and a non-invasive tool to monitor HIV-1 progression. In people living with HIV-1, an increase in the size and abundance of EVs is associated with a decline in the CD4/CD8 T cells ratio, a key marker of immune dysfunction. Analysis of host nucleic acids within EVs has revealed an enrichment of microRNA-155 (miR-155) during HIV-1 infection. Experiments have demonstrated that miR-155-rich EVs enhance HIV-1 infection in vitro. A humanized NSG-mouse model was established to assess the in vivo impact of miR-155-rich EVs. Co-production of the virus with miR-155-rich EVs heightened the viral load and lowered the CD4/CD8 ratio in the mice. Upon euthanasia, EVs were isolated from plasma for size and quantity assessment. Consistent with findings in individuals with HIV-1, increased EV size and abundance were inversely correlated with the CD4/CD8 ratio. Next, by using the virus co-product with EV-miR-155, we tested a DCIR inhibitor to limit infection and immune damage in a humanized mouse model. DCIR inhibition reduced infection and partially restored immune functions. Finally, viral particles and various EV subtypes can convey HIV-1 RNA. HIV-1 RNA was predominantly associated with large EVs (200-1000 nm) rather than small EVs (50-200 nm). Viral loads in large EVs strongly correlated with blood and tissue markers of immune activation. The humanized mice model has proven its applicability to studying the roles of EVs on HIV-1 infection and investigating the impact of DCIR inhibition.

MicroRNAs (miRNAs) hold significant promise as circulating cancer biomarkers and unlike many other molecular markers, they can provide valuable insights that extend beyond tumour biology. The expression of circulating miRNAs may parallel the cellular composition and dynamic activity within the tumour microenvironment and reveal systemic immune responses. The functional complexity of miRNAs-where a single miRNA can regulate multiple messenger RNAs (mRNAs) to fine tune fundamental processes, and a single mRNA can be targeted by multiple miRNAs-underscores their broad significance and impact. However, this complexity poses significant challenges for translating miRNA research into clinical practice. In melanoma, specific miRNA signatures have shown notable diagnostic, prognostic and predictive value, with lineage-specific and immune-related miRNAs frequently identified as valuable markers. In this review, we explore the role of circulating miRNAs as potential biomarkers in melanoma, and highlight the current status and advances required to translate miRNA research into therapeutic opportunities.

MicroRNAs (miRNAs) are ~22-nucleotide small non-coding RNAs that play critical roles in gene regulation. The discovery of miRNAs in Caenorhabditis elegans in 1993 by the research groups of Victor Ambros and Gary Ruvkun opened a new era in RNA research. Typically, miRNAs act as negative regulators of gene expression by binding to complementary sequences within the 3' untranslated regions of their target mRNAs. This interaction results in translational repression and/or target destabilization. The expression levels and activities of miRNAs are fine-tuned by multiple factors, including the miRNA biogenesis pathway, variability in target recognition, super-enhancers, post-transcriptional modifications, and target-directed miRNA degradation. Together, these factors form complex mechanisms that govern gene regulation and underlie several pathological conditions, including Argonaute syndrome, genetic diseases driven by super-enhancer-associated miRNAs, and miRNA-deadenylation-associated bone marrow failure syndromes. In addition, as miRNA genes have evolved rapidly in vertebrates, miRNA regulation in the brain is characterized by several unique features. In this review, we summarize recent insights into the role of miRNAs in human diseases, focusing on miRNA biogenesis; regulatory mechanisms, such as super-enhancers; and the impact of post-transcriptional modifications. By exploring these mechanisms, we highlight the intricate and multifaceted roles of miRNAs in health and disease.

The bulk of RNA produced from the genome of complex organisms consists of a very large number of transcripts lacking protein translational potential and collectively known as noncoding RNAs (ncRNAs). Initially thought to be mere products of spurious transcriptional noise, ncRNAs are now universally recognized as pivotal players in cell regulatory networks across a broad spectrum of biological processes. Owing to their critical regulatory roles, ncRNA dysfunction is closely associated with the etiopathogenesis of various human malignancies, including cancer. As such, ncRNAs represent valuable diagnostic biomarkers as well as potential targets for innovative therapeutic intervention. In this review, we focus on microRNAs (miRNAs) and long noncoding RNAs (lncRNAs), the two most extensively studied classes in the field of ncRNA biology. After outlining key concepts of miRNA and lncRNA biogenesis pathways, we examine their multiple roles in mediating epigenetic regulation of gene expression and chromatin organization. Finally, by providing numerous examples of specific miRNAs and lncRNAs, we discuss how dysregulation of these mechanisms contributes to the onset and/or progression of various human diseases.

Insect metamorphosis is a complex developmental process regulated by microRNAs (miRNAs) and hormonal signaling pathways. Key genes driving insect ontogenic changes are precisely modulated by miRNAs, which interact with 20-hydroxyecdysone (20E) and juvenile hormone (JH) to coordinate developmental transitions. Over the past decade, significant progress has been made in understanding miRNA biogenesis, their regulatory roles in gene expression, and their involvement in critical biological processes, including metamorphosis and chitin metabolism. miRNAs are now recognized as essential regulators of chitin metabolism and hormonal signaling, ensuring precise control of insect development. Disrupting the expression of participating genes in hormone signaling pathways through miRNAs leads to aberrant metamorphosis and consequent lethal outcomes, highlighting their potential as targets for pest control. This review summarizes current advances in miRNA-mediated regulation of insect metamorphosis and chitin metabolism, with a focus on their interactions with 20E and JH signaling pathways. By integrating recent findings, we provide insights into the molecular mechanisms underlying miRNA function in developmental transitions and their potential applications in insect pest management strategies. © 2025 Society of Chemical Industry.

MicroRNA-related single nucleotide polymorphisms (miR-SNPs) are promising biomarkers for cancer diagnostics, yet accurate detection methods remain limited. Here, we introduce a ligation-triggered Pyrococcus furiosus Argonaute (PfAgo) cleavage (LTAC) strategy for the sensitive detection of miR-SNPs, demonstrated using the rs11614913 SNP in miR-196a2, which is associated with nonsmall cell lung cancer (NSCLC). The mutant miR-196a2T serves as a scaffold for the formation of guide DNA (gDNA) catalyzed by the SplintR ligase, leading to PfAgo activation and enhanced fluorescence. In contrast, wild-type miR-196a2C cannot facilitate gDNA formation and thus fails to activate PfAgo. This method exhibits a linear relationship with the logarithm of the miR-196a2T concentration over a range of 0.2 pM to 100 nM, achieving a low detection limit of 0.15 pM. Analysis of NSCLC patient samples using LTAC reveals elevated levels of the rs11614913 SNP in miR-196a2 compared to healthy controls, underscoring the diagnostic potential of LTAC.

Circular RNAs (circRNAs) make up approximately 10% of the human transcriptome. CircRNAs belong to the broad group of non-coding RNAs and characteristically are formed by backsplicing into a stable circular loop. Their main role is to regulate transcription through the inhibition of miRNAs' expression, termed miRNA sponging. CircRNAs promote tumorigenesis/lymphomagenesis by competitively binding to miRNAs at miRNA binding sites. In diffuse large B-cell lymphoma (DLBCL), several circRNAs have been identified and their expression is related to both progression and response to therapy. DLBCL is the most prevalent and aggressive subtype of B-cell lymphomas and accounts for about 25% to 30% of all non-Hodgkin lymphomas. DLBCL displays great heterogeneity concerning histopathology, biology, and genetics. Patients who have relapsed or have refractory disease after first-line therapy have a very poor prognosis, demonstrating an important unmet need for new treatment options. As more circRNAs are identified in the future, we will better understand their biological roles and potential use in treating cancer, including DLBCL. For example, circAmotl1 promotes nuclear translocation of MYC and upregulation of translational targets of MYC, thus enhancing lymphomagenesis. Another example is circAPC, which is significantly downregulated in DLBCL and correlates with disease aggressiveness and poor prognosis. CircAPC increases expression of the host gene adenomatous polyposis coli (APC), and in doing so inactivates the canonical Wnt/β-catenin signaling and restrains DLBCL growth. MiRNAs belong to the non-coding regulatory molecules that significantly contribute to lymphomagenesis through their target mRNAs. In DLBCL, among the highly expressed miRNAs, are miR-155-5p and miR-21-5p, which regulate NF-ĸB and PI3K/AKT signaling pathways. The aim of this review is to describe the function and mechanism of regulation of circRNAs on miRNAs' expression in DLBCL. This will help us to better understand the regulatory network of circRNA/miRNA/mRNA, and to propose novel therapeutic targets to treat DLBCL.

BACKGROUND B: acterial leaf streak (BLS) is a bacterial disease that severely affects rice leaves, leading to significant yield reductions. microRNAs (miRNAs) are short non-coding RNAs extensively involved in the growth, development, and stress responses of plants and animals. However, miRNAs that regulate the response of rice to bacterial leaf streak are still relatively scarce. RESULTS: The indica rice variety Dular exhibits resistance to BLS, whereas the variety 9311 is highly susceptible to the disease. By conducting miRNA sequencing and transcriptome sequencing on both Dular and 9311 before and after BLS inoculation, we identified 19 miRNAs that were significantly downregulated at both 12 and 24 h post-inoculation in Dular, and 9 miRNAs that were significantly upregulated at the same time points in 9311. Additionally, through degradome sequencing, we identified 23 miRNA- mRNA regulatory modules that likely play crucial roles in rice resistance to BLS, and 4 miRNA- mRNA regulatory modules that may be important in rice susceptibility to the disease. DISCUSSION: Current studies on rice disease resistance miRNAs primarily focus on those involved in resistance to rice blast and bacterial blight, with the miRNA-target mRNA regulatory mechanisms for BLS remaining unclear. This study has identified miRNA-mRNA modules that may play significant roles in rice responses to BLS, contributing to the understanding of the miRNA regulatory network involved in rice defense against BLS infection.

Clear-cell renal cell carcinoma (ccRCC) is a common urological malignancy with an increasing incidence. The development of molecular biomarkers that can predict the response to treatment and guide personalized therapy selection would substantially improve patient outcomes. Dysregulation of non-coding RNA (ncRNA) has been shown to have a role in the pathogenesis of ccRCC. Thus, an increasing number of studies are being carried out with a focus on the identification of ncRNA biomarkers in ccRCC tissue samples and the connection of these markers with patients' prognosis, pathological stage and grade (including metastatic potential), and therapy outcome. RNA sequencing analysis led to the identification of several ncRNA biomarkers that are dysregulated in ccRCC and might have a role in ccRCC development. These ncRNAs have the potential to be prognostic and predictive biomarkers for ccRCC, with prospective applications in personalized treatment selection. Research on ncRNA biomarkers in ccRCC is advancing, but clinical implementation remains preliminary owing to challenges in validation, standardization and reproducibility. Comprehensive studies and integration of ncRNAs into clinical trials are essential to accelerate the clinical use of these biomarkers.

Systemic administration of induced pluripotent stem cell-derived mesenchymal stem cells (iPS-MSCs) has a therapeutic effect on myocardial ischemia. However, the therapeutic mechanism underlying systemic iPS-MSC-based therapy for ischemic cardiomyopathy (ICM) remains unclear. We investigated the therapeutic effects of iPS-MSCs through extracellular vesicle (EV)-mediated tissue repair in a rat model of ICM.

A rat ICM model was created by left anterior descending coronary artery ligation. iPS-MSCs were administered intravenously every week for four weeks in the iPS-MSC group, whereas saline was administered to the control group. Alix, a protein involved in the biogenesis of EVs, was knocked down, and Alix-knockdown iPS-MSCs were administered to the siAlix group. We analyzed sequential cardiac function using echocardiography, histological analysis, cell tracking analysis with fluorescent dyes, and comprehensive RNA sequencing of the border zone of the myocardium after treatment.

Left ventricular ejection fraction (LVEF) was significantly improved in the iPS-MSC group compared with that in the control group. In the siAlix group, LVEF was significantly lower than that in the iPS-MSC group. Histological analysis showed a significant decrease in fibrosis area and significant increase in microvascular density in the iPS-MSC group. A cell-tracking assay revealed iPS-MSC accumulation in the border zone of the myocardium during the acute phase. Comprehensive microRNA sequencing analysis revealed that EVs from iPS-MSCs contained miRNAs associated with anti-fibrosis and angiogenesis. Gene ontology analysis of differentially expressed genes in myocardial tissue also showed upregulation of pathways related to antifibrosis and neovascularization and downregulation of pathways linked to inflammation and T-cell differentiation.

Systemic administration of iPS-MSCs improved cardiac function through EV-mediated angiogenetic and antifibrotic effects in an ICM, suggesting the clinical possibility of treating chronic heart failure.

Rheumatoid arthritis (RA) is a chronic autoimmune disorder characterized by inflammatory joint damage. Recent studies have focused on the significance of microRNAs (miRNAs) in the pathogenesis of RA. Mesenchymal stem cells (MSCs) have emerged as a potential therapeutic option for RA based on their regenerative and immunomodulatory properties. MSCs release extracellular vesicles (EVs) containing miRNAs that can modulate immune and inflammatory responses. This article provides a comprehensive overview of the current evidence on the existence of various MSCs-derived miRNAs involved in the pathophysiology, characterization, and treatment of RA. An overview of the miRNA profiles in MSC-EVs is provided, along with an examination of their impact on various cell types implicated in RA pathogenesis, including synovial fibroblasts, macrophages, and T cells. Furthermore, the therapeutic capability of MSC-EVs for miRNA-based therapies in RA is discussed. In total, this review can present an extensive view of the complex interaction between EVs and MSC-derived miRNAs in RA and thus suggest valuable strategies for developing new therapeutic approaches to target this debilitating disease.

Accurate quantification of microRNA (miRNA) is of great significance because it provides opportunities for the accurate early diagnosis of a series of human diseases including cancers. Currently, complicated nucleic acid amplification technologies are always required for the highly sensitive miRNA detection. The introduction of nucleic acid signal amplification coupled with various enzymes will inevitably lead to tedious work and increase the complexity of the analysis process. It is still urgently desired to develop enzyme-free yet sensitive assays that enable the sensitive analysis of miRNA in complicated biological samples.

A single microbead (MB)-based localized catalytic hairpin assembly (CHA) strategy is proposed for the sensitive analysis of microRNA (miRNA). This rationally designed CHA strategy allows target miRNA to walk only on a single MB which can create a micro-amplification zone, initiating a highly efficient localized CHA reaction, generating a large number of fluorescent DNA duplexes on the surface of single MB. The efficient localized CHA on single MB can not only greatly suppress the nonspecific reaction between two hairpin probes, thus decreasing the background signal, but also greatly enhance the brightness of MB owing to the highly-concentrated fluorescence enrichment on only one MB. Therefore, highly sensitive quantification of miRNA has been achieved by measuring the fluorescence signal on MB using a confocal fluorescence microscope. This new strategy exhibits a detection limit of 1.09 pM for let-7a detection, and enables high specificity of distinguishing homologous miRNA family members.

This is the first report by only using one single MB as a carrier to conduct localized CHA, rendering highly-concentrated fluorescence enrichment on only one MB and a dramatic increase in sensitivity. This single MB-based localized CHA strategy has been successfully applied to the accurate analysis of miRNA target in complex biological sample.

Recent studies have illuminated the complexities of treating advanced bladder cancer (BCa), underscoring the importance of comprehending its molecular mechanisms for creating novel therapies. While the role of Karyopherin a2 (KPNA2) in promoting BCa growth is established, the precise mechanism remains elusive.

To investigate the regulatory role of KPNA2 in BCa, we employed a comprehensive approach integrating clinical case data and bioinformatics analysis to evaluate the expression of KPNA2 in BCa tissues. Mechanisms promoting cancer by KPNA2 were examined using both in vivo and in vitro models.

Our research reveals that miR-26b-5p acts as an anticancer factor by targeting and inhibiting KPNA2 expression. Furthermore, we have observed that the interaction between KPNA2 and Kinesin Family Member C1 (KIFC1) facilitates the transition of BCa cells into the G2/M phase, thereby promoting tumor advancement via activation of the Phosphoinositide 3-kinase (PI3K)- Protein Kinase B (AKT) pathway. Importantly, this investigation is the first to identify KPNA2 expression in exosomes originating from BCa tissues. Plasma exosomes from patients with BCa exhibited notably increased levels of KPNA2 compared with healthy controls, suggesting KPNA2 as a potential new tumor indicator. Additionally, KPNA2 from BCa cells triggered the conversion of fibroblasts into cancer-associated fibroblasts (CAFs), which secreted elevated levels of interleukin-6 (IL-6), contributing to a tumor-supporting environment.

These findings suggest that KPNA2 is a key gene that promotes BCa progression, can potentially be a novel tumor marker, and may serve as a new therapeutic target for BCa.

This study aimed to explore the mechanisms through which microRNAs (miRNAs) regulate 5-fluorouracil (5-FU) sensitivity in colorectal cancer (CRC) using organoid models. Fresh tissue samples from CRC tumors were collected, and CRC organoids were isolated and cultured. The consistency between CRC organoids and their derived tissues was validated. CRC organoids were treated with 5-FU, and ATP activity was measured. High-throughput sequencing of CRC organoids, combined with Gene Expression Omnibus (GEO) data analysis, was performed to examine miRNA expression following 5-FU treatment. Next, we investigated the cellular function of miR-526b-5p in CRC organoids and cells. Dual-luciferase reporter assays validated the binding of miR-526b-5p to the 3' UTR of TP53 mRNA. We successfully established CRC organoids that exhibited characteristics consistent with their source tissues. 5-FU treatment suppressed the proliferation and ATP activity of CRC organoids. High-throughput sequencing of CRC organoids, combined with GEO data analysis and quantitative reverse transcription polymerase chain reaction (qRT-PCR) validation, revealed that hsa-miR-526b-5p levels were elevated following 5-FU treatment in CRC organoids and cells. Furthermore, hsa-miR-526b-5p was upregulated in CRC tissues compared to adjacent normal tissues, correlating with poor survival in CRC patients. Overexpression of hsa-miR-526b-5p mitigated the inhibitory effects of 5-FU on CRC organoid proliferation, migration, invasion, and ferroptosis. In contrast, silencing of hsa-miR-526b-5p impaired cell function and ferroptosis. Additionally, overexpression of hsa-miR-526b-5p decreased TP53 mRNA and protein levels while increasing the expression of SLC7A11 mRNA and protein. Silencing of hsa-miR-526b-5p resulted in the opposite effect. hsa-miR-526b-5p directly targeted and inhibited TP53 expression. Overexpression of TP53 diminished the promotive effect of hsa-miR-526b-5p on ferroptosis-related proteins GPX4 and SLC7A11, whereas inhibition of TP53 reversed the impact of hsa-miR-526b-5p silencing. Our study demonstrates that hsa-miR-526b-5p targets TP53 to regulate 5-FU sensitivity in CRC through the ferroptosis pathway based on CRC organoid models.

Chronic kidney disease (CKD) is a prevalent health condition characterized by gradual kidney function loss. Early detection is crucial for the effective management and treatment of CKD. A promising biomarker for various diseases, including chronic kidney disease, is microRNAs (miRNAs), which are becoming increasingly important due to their stability and differential expression in various disease-related states, including CKD. Recent developments in microRNA biosensors have made it possible to detect miRNAs associated with CKD in a sensitive and specific manner. This review article discusses the current state of microRNA biosensors for detecting CKD and highlights their potential applications in clinical settings. Various microRNA biosensors, including electrochemical, optical, and nanomaterial-based sensors, are explored for their ability to detect specific miRNAs linked to CKD progression. The advantages and limitations of these biosensors are evaluated, focusing on factors such as sensitivity, specificity, and ease of use. Overall, microRNA biosensors are promising diagnostic tools for early detection of CKD. However, challenges such as standardizing protocols, validating in large cohorts, and translating to clinical practice remain to be addressed. Future research efforts should aim to overcome these limitations to fully realize the potential of microRNA biosensors in improving the diagnosis and management of CKD.

Recent advancements in microRNAs (miRNAs) research have revealed their key roles in both normal physiological processes and pathological conditions, leading to potential applications in diagnostics and therapeutics. However, the path forward is fraught with several scientific and technical challenges. This review article briefly explores the milestones of the discovery, biogenesis, functions, and application for clinical diagnostic and therapeutic strategies of miRNAs. The potential challenges and future directions are also discussed to fully harness their capabilities.

In recent years, the Japanese population has been aging and the risk of contracting various age-related diseases has increased. Thus, there is a need to analyze components that are characteristic of aging and examine their association with diseases to detect age-related diseases at an early stage. In the present study, microRNAs (miRNAs/miRs) in serum extracellular vesicles (EVs) of 82-102-week-old mice were analyzed to identify miRNAs characteristic of aging. Increased expression of mmu-miR-21a-5p was observed. These miRNAs may be derived from senescent vascular endothelial cells, and RNA-sequencing data (GSE130727) of HUVECs induced to senesce by 4 Gy of radiation revealed that the miRNAs were involved in the cell cycle and DNA repair. Annotations to senescence-related pathways were also identified. Reduced expression of the miR-21-5p target gene, which has an identical sequence in humans and mice, was confirmed. In HUVECs induced to age under similar conditions, increased senescence-associated β-galactosidase activity and increased intracellular miR-21-5p expression were observed. A portion of the miR-21-5p was secreted extracellularly by internalizing tetraspanin-positive EVs, and miR-21-5p was secreted into the extracellular space. The present study also demonstrated that miR-21-5p expression was upregulated and extracellular secretion of miR-21-5p was enhanced during vascular endothelial cell senescence. These findings suggested that increased serum miR-21-5p represents a biomarker for vascular endothelial cell senescence.

The enzyme-free amplification technique using the Hybridization Chain Reaction (HCR) is gaining traction for its efficiency in miRNA analysis. Conventional HCR (C-HCR) with hairpin probes faces challenges due to enzymatic degradation in body fluids, leading to potential false-positive results. This study addresses the critical need for a more reliable method that resists enzymatic breakdown and improves diagnostic accuracy for detecting miRNA related to ischemic stroke. We have developed a novel DNA tetrahedral nanostructures-mediated HCR (DTN-HCR) platform for the precise detection of microRNA-25 (miR-25), a biomarker for ischemic stroke. Incorporating two unique DNA tetrahedral nanostructures with embedded hairpin structures (DTN-HP1 and DTN-HP2), this platform activates upon miR-25 binding, initiating a robust DTN-HCR reaction. This reaction forms extensive DNA tetrahedron clusters that significantly boost the fluorescence signal, enabling detection thresholds as low as 5.4 pM. The method showcases exceptional specificity by distinguishing target miRNA from close analogues and maintains structural integrity against DNase I and fetal bovine serum (FBS), verified through polyacrylamide gel electrophoresis (PAGE). It successfully differentiates ischemic stroke patients from healthy controls by analyzing peripheral blood-derived miRNAs. This study concludes that the DTN-HCR platform substantially enhances the specificity and stability of miRNA detection, marking a significant advancement in non-enzymatic miRNA analysis techniques. With its capability to accurately identify ischemic stroke biomarkers at very low concentrations and its resistance to enzymatic degradation, the DTN-HCR method presents a valuable diagnostic tool for ischemic stroke, potentially improving early detection and monitoring in a clinical environment.

Fluorogenic RNA aptamers have various applications, including use as fluorescent tags for imaging RNA trafficking and as indicators of RNA-based sensors that exhibit fluorescence upon binding small-molecule fluorophores in living cells. Current fluorogenic RNA:fluorophore complexes typically emit visible fluorescence. However, it is challenging to develop fluorogenic RNA with near-infrared (NIR) fluorescence for in vivo imaging and sensing studies. To address this issue, we identify and modulate red fluorescent protein-like fluorophores to bind Squash, a highly folded fluorogenic RNA. One of these fluorophores, DFQL-1T, exhibits photostable NIR fluorescence when bound to Squash, enabling RNA visualization in living mammalian cells and mice. With Squash:DFQL-1T complexes, we generate RNA-based sensors for detecting non-coding RNAs and small molecule targets in living mammalian cells and in mice. These studies reveal a fluorogenic RNA:fluorophore complex that can be readily developed into NIR fluorescent RNA tags for in vivo imaging and sensing.

Periodontitis is a chronic inflammatory disease that leads to periodontal tissue damage and tooth loss. Therefore, controlling inflammatory bone loss and promoting osteogenesis is a crucial challenge clinically. MicroRNA (miRNA) based gene therapy has shown substantial prospects in recent years, but its application has been limited due to structural instability and easy degradation by enzymes. Research has shown that miRNA-200c is regarded as a key miRNA by regulating multiple signaling pathways during the process of bone resorption. Tetrahedral framework nucleic acid (tFNA) can be considered an ideal carrier of miRNA due to its good tissue permeability, cell uptake efficiency, and biocompatibility. This study developed a tFNA system carrying miR-200c, named T-200c, to exert various biological effects in human periodontal ligament stem cells (PDLSCs). The activation of the NF-κB pathway is diminished, whereas the Akt/β-catenin pathway is enhanced, resulting in a notable decrease in the release of diverse inflammatory mediators and cellular reactive oxygen species. This modulation fosters cell proliferation and osteogenic differentiation, thereby rejuvenating the functionality of PDLSCs. These changes offer a viable alternative for the treatment of periodontitis and the regeneration of periodontal tissues.

Non-coding RNAs (ncRNAs) play crucial roles in gene expression regulation, translation, and disease development, including cancer. They are classified by size in short and long non-coding RNAs. This chapter focuses on the functional implications of adenosine-to-inosine (A-to-I) RNA editing in both short (e.g., miRNAs) and long ncRNAs. RNA editing dynamically alters the sequence and structure of primary transcripts, impacting ncRNA biogenesis and function. Notable findings include the role of miRNA editing in promoting glioblastoma invasiveness, characterizing RNA editing hotspots across cancers, and its implications in thyroid cancer and ischemia. This chapter also highlights bioinformatics resources and next-generation sequencing (NGS) technologies that enable comprehensive ncRNAome studies and genome-wide RNA editing detection. Dysregulation of RNA editing machinery has been linked to various human diseases, emphasizing the potential of RNA editing as a biomarker and therapeutic target. This overview integrates current knowledge and computational tools for studying ncRNA editing, providing insights into its biological significance and clinical applications.

Detection of microRNAs (miRNAs) in the serum is an effective liquid biopsy technique for cancer diagnosis. However, conventional diagnostic methods are time-consuming and complex. Therefore, in this study, we established a signaling probe-based DNA microarray system for miRNA detection. PCR, fluorescence labeling, and washing are not necessary for signaling probes. Four probes were designed using different miRNAs as diagnostic cancer markers. The developed system is useful for various miRNAs, regardless of their target lengths (18-26-mer) and GC content (36%-89%). Here, all the assays were performed within 40 min. Overall, our signaling probe-based DNA hybridization system facilitates the simple and rapid detection of serum miRNAs without the need for gene amplification, fluorescence labeling and washing.

Our study aimed to explore the specific functions and potential mechanisms of miR-224-5p in non-small cell lung cancer (NSCLC).

We first analyzed the expression of miR-224-5p in NSCLC patients and cell lines through the GEO database and qRT-PCR analysis. Then, we used MTT assays, wound healing assays, Transwell assays, and western blotting to evaluate the effects of miR-224-5p on NSCLC cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT). Furthermore, we used a xenograft tumor model to evaluate the effect of miR-224-5p on NSCLC tumor growth. Potential binding targets of miR-224-5p were further identified through the target prediction databases, and the relationships between miR-224-5p, its targets, and downstream signaling pathways were further verified using luciferase reporter gene assays and western blotting.

The GEO database and qRT-PCR analysis indicated that miR-224-5p was significantly downregulated in NSCLC patients and cell lines. Functional assays indicated that inhibiting miR-224-5p could enhance the proliferation, migration, invasion, and EMT of NSCLC cells, as well as accelerate tumor growth. In contrast, overexpression of miR-224-5p inhibited these processes. We identified IL6ST (interleukin 6 signal transducer) as a binding target of miR-224-5p. We observed that miR-224-5p could bind to and inhibit IL6ST expression and JAK2/STAT3 signaling pathway, and the inhibition of NSCLC tumor growth and JAK2/STAT3 pathway by miR-224-5p could be reversed by IL6ST overexpression.

Our study demonstrated that miR-224-5p inhibited NSCLC by targeting IL6ST, thereby downregulating the JAK2/STAT3 signaling pathway.

The genesis of human disease lies in our evolutionary past. Evolution has featured a general trend towards increased morphological complexity, partly conferred by expansion in gene regulatory capacity via microRNA (miRNA) innovation. Many human diseases are directly related to the evolved roles of these miRNAs, and miRNA-based therapies are emerging as an appealing strategy for precision medicine. We focus on three categories of human disease - cancer, inflammation-linked pathologies, and neurological disorders - which are highly prevalent and are associated with substantial disease burden worldwide. In each category we discuss the pathogenic roles of miRNAs in the context of their evolved functions, as well as current and potential advances in targeting these miRNAs for disease therapy.

MicroRNA molecules have been shown to play various significant roles in many physiological and pathophysiological processes in living organisms. The tremendous interest in these molecules has led to the significant development and constant release of a number of computational tools useful for basic as well as advanced miRNA-related analyses. These approaches have various constantly evolving utilities, such as detection, target prediction, functional annotation, and many others. In this chapter, we provide an overview of several computational tools useful for broadly defined plant miRNA analysis. We have added to the Tools4miRs new databases that provide extensive information on small noncoding RNA sequences. Additionally, several tools within the platform have been updated, now featuring comprehensive references and accessible links, ensuring users have access to the most recent and relevant research findings.

MicroRNAs (miRNAs), a distinct category of non-coding RNAs, exert multifaceted regulatory functions in a variety of organisms, including humans, animals, and plants. The inventory of identified miRNAs stands at approximately 60,000 among all species and 1,926 in Homo sapiens manifests miRNA expression. Their theranostic role has been explored by researchers over the last few decades, positioning them as prominent therapeutic targets as our understanding of RNA targeting advances. However, limited availability of experimentally determined miRNA structures has constrained drug discovery efforts relying on virtual screening or computational methods, including machine learning and artificial intelligence.

To address this lacuna, miRVim has been developed, providing a repository of human miRNA structures derived from both two-dimensional (MXFold2, CentroidFold, and RNAFold) and three-dimensional (RNAComposer and 3dRNA) structure prediction algorithms, in addition to experimentally available structures from the RCSB PDB repository.

miRVim contains 13,971 predicted secondary structures and 17,045 predicted three-dimensional structures filling the gap of unavailability of miRNA structure data bank. This database aims to facilitate computational data analysis for drug discovery, opening new avenues for advancing technologies such as machine learning-based predictions in the field of RNA biology.

The publicly accessible structures provided by miRVim, available at https://mirna.in/miRVim, offer a valuable resource for the research community, advancing the field of miRNA-related computational analysis and drug discovery.

In the face of global health challenges posed by infectious diseases and the emergence of drug-resistant pathogens, the exploration of cellular non-coding RNA (ncRNA) networks has unveiled new dimensions in infection research. Particularly microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) have emerged as instrumental players in ensuring a balance between protection against hyper-inflammatory conditions and the effective elimination of pathogens. Specifically, ncRNAs, such as the miRNA miR-155 or the lncRNAs MaIL1 (macrophage interferon-regulatory lncRNA 1), and LUCAT1 (lung cancer-associated transcript 1) have been recurrently linked to infectious and inflammatory diseases. Together with other ncRNAs, discussed in this chapter, they form a complex regulatory network shaping the host response to pathogens. Additionally, some pathogens exploit these ncRNAs to establish and sustain infections, underscoring their dual roles in host protection and colonization. Despite the substantial progress made, the vast majority of ncRNA loci remains unexplored, with ongoing research likely to reveal novel ncRNA categories and expand our understanding of their roles in infections. This chapter consolidates current insights into ncRNA-mediated regulatory networks, highlighting their contributions to severe diseases and their potential as targets and biomarkers for innovative therapeutic strategies.

MicroRNAs (miRNA,miRs) are small noncoding RNAs that are ubiquitously expressed in all mammalian cells. Their primary function is the regulation of nascent RNA transcripts by direct binding to regions on the target. There is now exciting data to suggest that these miRNAs can bind to other miRNAs, and this may have a broader impact on gene regulation in disease states. The oncomiR miR-21 is one of the highest-expressing miRNAs in cancer cells, and in this study, we characterise which miRNAs could be potential targets of miR-21. In cancer cells delivered with a miR-21 mimic, there was an observable shift of the miRNA milieu. We demonstrate that the miR-17-92a cluster, which harbours six miRNA members, may be a target for miR-21 regulation. Additionally, the primary transcript of miR-17-92a was reduced in the presence of miR-21. In the broader context of miR:miR regulation, overexpression of miR-21 shifted the expression of more than 150 miRNAs, including those known to regulate genes in cancer pathways such as the MAPK signalling and FoxO pathways. This study expands upon our limited understanding of miR:miR regulatory network and reinforces the concept that miRNAs can regulate each other, thereby influencing broader gene networks.

Epigenetics plays a vital role in corneal health and diseases. Epigenetic changes regulate the expression of genes by altering the accessibility of chromatin via histone modifications, DNA methylation and miRNAs without altering DNA sequence. Ocular trauma and infections are common causes of corneal damage, vision impairment, and mono/bilateral blindness worldwide. Mounting literature shows that epigenetic modifications can modulate corneal clarity, function, and pathogenesis including inflammation, wound healing, fibrosis, and neovascularization. Additionally, epigenetic modifications can be targeted to reverse corneal pathologies and develop interventional therapies. However, current understanding on how epigenetic modifications lead to corneal abnormalities and diseases is limited. This review provides in-depth knowledge and mechanistic understanding of epigenetics alterations in corneal pathogenesis, and information on potential epigenetic targets for treatment of corneal diseases.

Fasciolosis is a neglected tropical disease caused by helminth parasites of the genus Fasciola spp., including Fasciola hepatica (F. hepatica) and Fasciola gigantica (F. gigantica), being a major zoonotic problem of human and animal health. Its control with antihelminthics is becoming ineffective due to the increase in parasite resistance. Developing new therapeutic protocols is crucial to a deeper knowledge of the molecular bases in the host-parasite interactions. The high-throughput omics technologies have dramatically provided unprecedented insights into the complexity of the molecular host-parasite crosstalk. MicroRNAs (miRNAs) are key players as critical regulators in numerous biological processes, modifying the gene expression of cells by degradation of messenger RNA (mRNA), regulating transcription and translation functions, protein positioning, cell cycle integrity, differentiation and apoptosis. The large-scale exploration of miRNAs, including the miRNome, has offered great scientific knowledge of steps in fasciolosis, further scrutinizing the pathogenesis, the growth and development of their strains and their interaction with the host for the survival of the different parasite stages. This review compiles the updated knowledge related to miRNAs involved in fasciolosis and the generated miRNome, highlighting the importance of these key molecules in the host-parasite interactions and the pathogenesis of Fasciola spp. directing towards the development of new biotherapeutic protocols for the control of fasciolosis.