Shifting from the inflammatory to the proliferative phase represents a pivotal step during managing diabetic foot ulcers (DFUs); however, existing medical interventions remain insufficient. MicroRNAs (miRs) highlight notable capacity for accelerating the repair process of DFUs. Previous research has demonstrated which miR-122-5p regulates matrix metalloproteinases under diabetic conditions, thereby influencing extracellular matrix dynamics.

To investigate the impact of miR-122-5p on the transition from the inflammatory to the proliferative stage in DFU.

Analysis for miR-122-5p expression in skin tissues from diabetic ulcer patients and mice was analyzed using quantitative real-time polymerase chain reaction (qRT-PCR). A diabetic wound healing model induced by streptozotocin was used, with mice receiving intradermal injections of adeno-associated virus -DJ encoding empty vector or miR-122. Skin tissues were retrieved at 3, 7, and 14 days after injury for gene expression analysis, histology, immunohistochemistry, and network studies. The study explored miR-122-5p’s role in macrophage-fibroblast interactions and its effect on transitioning from inflammation to proliferation in DFU healing.

High-throughput sequencing revealed miR-122-5p as crucial for DFU healing. qRT-PCR showed significant upregulation of miR-122-5p within diabetic skin among DFU individuals and mice. Western blot, along with immunohistochemical and enzyme-linked immunosorbent assay, demonstrating the upregulation of inflammatory mediators (hypoxia inducible factor-1α, matrix metalloproteinase 9, tumor necrosis factor-α) and reduced fibrosis markers (fibronectin 1, α-smooth muscle actin) by targeting vascular endothelial growth factor. Fluorescence in situ hybridization indicated its expression localized to epidermal keratinocytes and fibroblasts in diabetic mice. Immunofluorescence revealed enhanced increased presence of M1 macrophages and reduced M2 polarization, highlighting its role in inflammation. MiR-122-5p elevated inflammatory cytokine levels while suppressing fibrotic activity from fibroblasts exposed to macrophage-derived media, highlighting its pivotal role in regulating DFU healing.

MiR-122-5p impedes cutaneous healing of diabetic mice via enhancing inflammation and inhibiting fibrosis, offering insights into miR roles in human skin wound repair.

• MicroRNA-122-5p
• Diabetic foot ulcer
• Wound healing
• Inflammation
• Fibrosis

• infection
• innate immunity
• microRNAs
• porcine reproductive and respiratory syndrome virus
• viral genome

• Swine
• Animals
• Porcine respiratory and reproductive syndrome virus/genetics
• MicroRNAs/genetics
• MicroRNAs/metabolism
• Immunity, Innate
• Viral Proteins

• Biomarkers
• CircRNAs
• LncRNAs
• Metabolic diseases
• Non-coding RNAs
• Therapeutic targets
• miRNAs

• Overexpressed miRNAs
• anticancer
• antisense miRNAs
• cancer therapeutic
• miRNA dysregulation
• tumor suppressor genes

Hyperlipidemia is a common metabolic disorder with high morbidity and mortality, which brings heavy burden on social. Understanding its pathogenesis and finding its potential therapeutic targets are the focus of current research in this field. In recent years, an increasing number of studies have proved that miRNAs play vital roles in regulating lipid metabolism and were considered as promising therapeutic targets for hyperlipidemia and related diseases. It is demonstrated that miR-191, miR-222, miR-224, miR-27a, miR-378a-3p, miR-140-5p, miR-483, and miR-520d-5p were closely associated with the pathogenesis of hyperlipidemia. In this review, we provide brief overviews about advances in miRNAs in hyperlipidemia and its potential clinical application value.

• Animals
• Graft vs Host Disease/pathology
• Hematopoietic Stem Cell Transplantation/adverse effects
• Hypoxia
• Mice
• Mice, Knockout
• MicroRNAs/genetics

• R01 AI118305 NIAID NIH HHS
• R01 HL137373 NHLBI NIH HHS
• R01 HL140953 NHLBI NIH HHS

Alzheimer’s disease (AD) is a neurodegenerative proteinopathic disease. The deposits of misfolded Amyloid β and Tau proteins in the brain of patients with AD suggest an imbalance in endoplasmic reticulum (ER) proteostasis. ER stress is due to accumulation of aberrant proteins in the ER lumen, which then leads to activation of three sensor protein pathways that ultimately evokes the adaptive mechanism of the unfolded protein response (UPR). The UPR mechanism operates via adaptive UPR and the apoptotic UPR. Adaptive UPR tries to restore imbalance in ER hemostasis by decreasing protein production, enhanced chaperone involvement to restore protein folding, misfolded protein decay by proteasome, and suppression of ribosomal translation ultimately relieving the excessive protein load in the ER. Subsequently, apoptotic UPR activated under severe ER stress conditions triggers cell death. MicroRNAs (miRNAs) are small non-coding protein causing dysregulated translational of mRNAs in a sequential manner. They are considered to be critical elements in the maintenance of numerous cellular activities, hemostasis, and developmental processes. Therefore, upregulation or downregulation of miRNA expression is implicated in several pathogenic processes. Evidence from scientific studies suggest a strong correlation between ER^UPR signaling and miRNA dysregulation but the research done is still dormant. In this review, we summarized the cross-talk between ER stress, and the UPR signaling processes and their role in AD pathology by scrutinizing and collecting information from original research and review articles.

• Umm Al-Qura University

• COVID-19
• MicroRNAs
• SARS-CoV-2
• biomarker
• gene regulation
• miRNA-based therapeutics

• COVID-19/genetics
• Humans
• MicroRNAs/genetics
• SARS-CoV-2

• Asthma
• Atopic dermatitis
• Dendritic cells
• Rhinitis
• Th2-disorder
• microRNA therapeutics

• androgen receptor signaling
• microRNAs
• prostate biology
• prostate cancer

• RNAi
• Rna therapeutics
• antisense RNA
• drug delivery
• miRNA

• Alternative Splicing/genetics
• Animals
• Gene Transfer Techniques
• Humans
• MicroRNAs/therapeutic use
• Models, Biological
• Oligonucleotides, Antisense/therapeutic use

Myotonic dystrophy involves two types of chronically debilitating rare neuromuscular diseases: type 1 (DM1) and type 2 (DM2). Both share similarities in molecular cause, clinical signs, and symptoms with DM2 patients usually displaying milder phenotypes. It is well documented that key clinical symptoms in DM are associated with a strong mis-regulation of RNA metabolism observed in patient’s cells. This mis-regulation is triggered by two leading DM-linked events: the sequestration of Muscleblind-like proteins (MBNL) and the mis-regulation of the CUGBP RNA-Binding Protein Elav-Like Family Member 1 (CELF1) that cause significant alterations to their important functions in RNA processing. It has been suggested that DM1 may be treatable through endogenous modulation of the expression of MBNL and CELF1 proteins. In this study, we analyzed the recent identification of the involvement of microRNA (miRNA) molecules in DM and focus on the modulation of these miRNAs to therapeutically restore normal MBNL or CELF1 function. We also discuss additional prospective miRNA targets, the use of miRNAs as disease biomarkers, and additional promising miRNA-based and miRNA-targeting drug development strategies. This review provides a unifying overview of the dispersed data on miRNA available in the context of DM.

• CELF1
• MBNL proteins
• alternative splicing
• antisense oligonucleotides
• miRNA-based drug
• miRNA-targeting drug
• microRNA
• myotonic dystrophy

• Alternative Splicing
• Animals
• CELF1 Protein/genetics
• Drug Discovery
• Gene Expression Regulation
• Genetic Therapy
• Humans
• MicroRNAs/genetics
• Myotonic Dystrophy/genetics
• Myotonic Dystrophy/therapy
• RNA-Binding Proteins/genetics

• T cells
• extracellular vesicles
• immunity
• infectious diseases
• microRNAs
• modulation

Accumulating evidence demonstrates that microRNA- (miR-) mediated posttranscriptional regulation plays an important role in autophagy in inflammatory bowel disease (IBD), a disease that is difficult to manage clinically because of the associated chronic recurrent nonspecific inflammation. Research indicates that microRNAs regulate autophagy via different pathways, playing an important role in the IBD process and providing a new perspective for IBD research. Related studies have shown that miR-142-3p, miR-320, miR-192, and miR-122 target NOD2, an IBD-relevant autophagy gene, to modulate autophagy in IBD. miR-142-3p, miR-93, miR-106B, miR-30C, miR-130a, miR-346, and miR-20a regulate autophagy by targeting ATG16L1 through several different pathways. miR-196 can downregulate IRGM and suppress autophagy by inhibiting the accumulation of LC3II. During the endoplasmic reticulum stress response, miR-665, miR-375, and miR-150 modulate autophagy by regulating the unfolded protein response, which may play an important role in IBD intestinal fibrosis. Regarding autophagy-related pathways, miR-146b, miR-221-5p, miR-132, miR-223, miR-155, and miR-21 regulate NF-κB or mTOR signaling to induce or inhibit autophagy in intestinal cells by releasing anti- or proinflammatory factors, respectively.

Cholangiocarcinoma (CCA) is an aggressive malignancy that arises from damaged epithelial cells, cholangiocytes, and possibly de-differentiated hepatocytes. CCA has a poor overall survival rate and limited therapeutic options. Based on this data, it is imperative that new diagnostic and therapeutic interventions be developed. Recent work has attempted to understand the pathological mechanisms driving CCA progression. Specifically, recent publications have delved into the role of cancer stem cells (CSCs), mesenchymal stem cells (MSCs), and microRNAs (miRNAs) during CCA pathology. CSCs are a specific subset of cells within the tumor environment that are derived from a cell with stem-like properties and have been shown to influence recurrence and chemoresistance during CCA. MSCs are known for their anti-inflammatory activity and have been postulated to influence malignancy during CCA, but little is known about their exact functions. miRNAs exert various functions via gene regulation at both the transcriptional and the translational levels, giving miRNAs diverse roles in CCA progression. Additionally, current miRNA-based therapeutic approaches are in clinical trials for various liver diseases, giving hope for similar approaches for CCA. However, the interactions among these three factors in the context of CCA are unknown. In this review, we focus on recently published data (within the last 3 years) that discuss the role of CSCs, MSCs, and miRNAs and their possible interactions during CCA pathogenesis.

• cancer stem cells
• cholangiocarcinoma
• mesenchymal stem cells
• microRNAs

• Cholangiopathies
• Diagnosis
• Therapy
• microRNAs

• AVI-4065
• DAA
• HCV
• ISIS-14803
• Miravirsen
• RG-101
• SPC3649
• TT-034
• life cycle
• translation inhibitors

The genus Enterovirus, a member of the Picornavirus family, are RNA viruses that can cause poliomyelitis, hand-food-mouth disease, viral meningitis or meningoencephalitis, viral myocarditis and so on. MicroRNAs are a class of highly conserved, small noncoding RNAs recognized as important regulators of gene expression. Recent studies found that MicroRNAs play a significant role in the infection of Enterovirus, such as enterovirus 71, coxsackievirus B3 and other Enterovirus. Enteroviral infection can alter the expression of cellular MicroRNAs, and cellular MicroRNAs can modulate viral pathogenesis and replication by regulating the expression level of viral or host's genes. Herein, this review summarizes the role of MicroRNAs in enteroviral infection.

• Enterovirus
• Infection
• MicroRNAs

• HCV replication
• Overexpression
• Pro-survival pathway
• miR-199a-5p

• Children
• Daclatasvir
• Efficacy
• Hepatitis C virus
• Interferon
• Ribavirin
• Safety
• Sofosbuvir
• Treatment

• Age Factors
• Animals
• Antiviral Agents/adverse effects
• Antiviral Agents/therapeutic use
• Drug Therapy, Combination
• Hepacivirus/drug effects
• Hepacivirus/genetics
• Hepacivirus/metabolism
• Hepatitis C, Chronic/diagnosis
• Hepatitis C, Chronic/drug therapy
• Hepatitis C, Chronic/virology
• Host-Pathogen Interactions
• Humans
• Molecular Targeted Therapy
• Pediatrics/standards
• Standard of Care
• Treatment Outcome