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Dhiman A, Choudhary D, Mehan S, Maurya PK, Sharma AK, Kumar A, Mukherjee R, Gupta S, Khan Z, Gupta GD, Narula AS. Therapeutic potential of Baicalin against experimental obsessive compulsive disorder: Evidence from CSF, blood plasma, and brain analysis. J Neuroimmunol 2025; 403:578598. [PMID: 40168745 DOI: 10.1016/j.jneuroim.2025.578598] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/22/2024] [Revised: 03/13/2025] [Accepted: 03/24/2025] [Indexed: 04/03/2025]
Abstract
Obsessive-Compulsive Disorder (OCD) is a complex neuropsychiatric condition characterized by recurrent obsessions and compulsions, significantly impacting an individual's functionality and quality of life. This study aimed to explore the neuroprotective and therapeutic potential of baicalin, a flavonoid with known antioxidant, anti-inflammatory, and neurotropic properties, in an animal model of OCD induced by 8-OH-DPAT (8HPAT). The research utilized in silico docking studies and in vivo experiments to assess baicalin's interactions with key intracellular targets: SIRT-1, Nrf2, HO-1, and PPAR-gamma, and its effects on neurochemical, neurobehavioral, and histopathological parameters. In silico results indicated a strong binding affinity of baicalin for SIRT-1, Nrf2, HO-1, and PPAR-gamma, suggesting potential regulatory roles in antioxidant and anti-inflammatory pathways. In-vivo findings demonstrated that baicalin, administered at doses of 50 mg/kg and 100 mg/kg, significantly alleviated OCD-like behaviours, including excessive lever pressing, marble burying, and compulsive checking. Baicalin treatment normalized serotonin and dopamine levels and reduced glutamate levels in the brain, restoring neurotransmitter balance. Furthermore, baicalin decreased inflammatory cytokines (TNF-alpha and IL-1 beta), improved complete blood count profile, and gross morphological and histopathological alterations by restoring neuronal density and cellular integrity in affected brain regions. Combining baicalin with fluvoxamine (10 mg/kg) showed synergistic effects, further enhancing neuroprotective outcomes. These results suggest that baicalin holds promise as a potential therapeutic agent for OCD, warranting further clinical investigation to explore its efficacy and underlying mechanisms in human subjects. The findings underscore the importance of targeting intracellular pathways and neurotransmitter systems in developing effective treatments for OCD and related neuropsychiatric disorders.
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Affiliation(s)
- Abhinay Dhiman
- Division of Neuroscience, Department of Pharmacology, ISF College of Pharmacy, Moga, Punjab, India (Affiliated to IK Gujral Punjab Technical University), Jalandhar, Punjab 144603, India
| | - Divya Choudhary
- Division of Neuroscience, Department of Pharmacology, ISF College of Pharmacy, Moga, Punjab, India (Affiliated to IK Gujral Punjab Technical University), Jalandhar, Punjab 144603, India
| | - Sidharth Mehan
- Division of Neuroscience, Department of Pharmacology, ISF College of Pharmacy, Moga, Punjab, India (Affiliated to IK Gujral Punjab Technical University), Jalandhar, Punjab 144603, India.
| | - Pankaj Kumar Maurya
- Division of Neuroscience, Department of Pharmacology, ISF College of Pharmacy, Moga, Punjab, India (Affiliated to IK Gujral Punjab Technical University), Jalandhar, Punjab 144603, India
| | - Arun Kumar Sharma
- Division of Neuroscience, Department of Pharmacology, ISF College of Pharmacy, Moga, Punjab, India (Affiliated to IK Gujral Punjab Technical University), Jalandhar, Punjab 144603, India
| | - Aakash Kumar
- Division of Neuroscience, Department of Pharmacology, ISF College of Pharmacy, Moga, Punjab, India (Affiliated to IK Gujral Punjab Technical University), Jalandhar, Punjab 144603, India
| | - Ritam Mukherjee
- Division of Neuroscience, Department of Pharmacology, ISF College of Pharmacy, Moga, Punjab, India (Affiliated to IK Gujral Punjab Technical University), Jalandhar, Punjab 144603, India
| | - Sumedha Gupta
- Division of Neuroscience, Department of Pharmacology, ISF College of Pharmacy, Moga, Punjab, India (Affiliated to IK Gujral Punjab Technical University), Jalandhar, Punjab 144603, India
| | - Zuber Khan
- Division of Neuroscience, Department of Pharmacology, ISF College of Pharmacy, Moga, Punjab, India (Affiliated to IK Gujral Punjab Technical University), Jalandhar, Punjab 144603, India
| | - Ghanshyam Das Gupta
- Department of Pharmaceutics, ISF College of Pharmacy, Moga, Punjab, India (Affiliated to IK Gujral Punjab Technical University), Jalandhar, Punjab 144603, India
| | - Acharan S Narula
- Narula Research, LLC, 107 Boulder Bluff, Chapel Hill, NC 27516, USA
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Zhang Y, Gong C, Tao L, Zhai J, Huang F, Zhang S. Involvement of SIRT1-mediated aging in liver diseases. Front Cell Dev Biol 2025; 13:1548015. [PMID: 40052151 PMCID: PMC11882576 DOI: 10.3389/fcell.2025.1548015] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/19/2024] [Accepted: 01/27/2025] [Indexed: 03/09/2025] Open
Abstract
Liver disease is a significant global health issue, responsible for millions of deaths annually. Aging, characterized by the gradual decline in cellular and physiological functions, impairs tissue regeneration, increases susceptibility to liver diseases, and leads to a decline in liver health. Silent information regulator 1 (SIRT1), a NAD⁺-dependent deacetylase, has emerged as a pivotal factor in modulating age-related changes in the liver. SIRT1 preserves liver function by regulating essential aging-related pathways, including telomere maintenance, epigenetic modifications, cellular senescence, intercellular communication, inflammation, and mitochondrial function. Notably, SIRT1 levels naturally decline with age, contributing to liver disease progression and increased vulnerability to injury. This review summarizes the regulatory role of SIRT1 in aging and its impact on liver diseases such as liver fibrosis, alcoholic associated liver disease (ALD), metabolic dysfunction-associated steatotic liver disease (MASLD), and metabolic dysfunction-associated steatohepatitis (MASH), hepatocellular carcinoma (HCC). We also discuss emerging therapeutic approaches, including SIRT1 activators, gene therapy, and nutritional interventions, which are evaluated for their potential to restore SIRT1 function and mitigate liver disease progression. Finally, we highlight future research directions to optimize SIRT1-targeted therapies for clinical applications in age-related liver conditions.
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Affiliation(s)
- Yueming Zhang
- Department of Clinical Pharmacy, The First Hospital of Jilin University, Changchun, China
| | - Chang Gong
- Department of Clinical Pharmacy, The First Hospital of Jilin University, Changchun, China
| | - Lina Tao
- Department of Pharmacy, The First Hospital of Jilin University, Changchun, China
| | - Jinghui Zhai
- Department of Clinical Pharmacy, The First Hospital of Jilin University, Changchun, China
| | - Fengwei Huang
- Department of Clinical Pharmacy, The First Hospital of Jilin University, Changchun, China
- College of Pharmacy, Jilin University, Changchun, Jilin, China
| | - Sixi Zhang
- Department of Clinical Pharmacy, The First Hospital of Jilin University, Changchun, China
- College of Pharmacy, Jilin University, Changchun, Jilin, China
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Wang LL, Lu YM, Wang YH, Wang YF, Fang RF, Sai WL, Yao DF, Yao M. Carnitine palmitoyltransferase-II inactivity promotes malignant progression of metabolic dysfunction-associated fatty liver disease via liver cancer stem cell activation. World J Gastroenterol 2024; 30:5055-5069. [PMID: 39713165 PMCID: PMC11612864 DOI: 10.3748/wjg.v30.i47.5055] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/09/2024] [Revised: 10/06/2024] [Accepted: 11/05/2024] [Indexed: 11/26/2024] Open
Abstract
BACKGROUND Metabolic dysfunction-associated fatty liver disease (MAFLD) is one of the main chronic liver diseases. However, the roles of mitochondrial carnitine palmitoyl transferase-II (CPT-II) downregulation and liver cancer stem cell (LCSC) activation remain to be identified. AIM To investigate the dynamic alterations in CPT-II inactivity and LCSC activation during the malignant progression of MAFLD. METHODS Dynamic models of mouse MAFLD were generated via the consumption of a high-fat diet or the addition of 2-fluorenylacetamide for hepatocarcinogenesis. The mice were divided into groups on the basis of hematoxylin and eosin staining. Biochemistries, CPT-II, intrahepatic T cells, and LCSCs were determined and confirmed in clinical samples. The mitochondrial membrane potential (MMP) was analyzed. Differentially expressed genes were screened via RNA sequencing and enriched in KEGG pathways or GO functions. RESULTS Dynamic models of MAFLD malignant transformation were successfully generated on the basis of pathological examination. Hepatic lipid accumulation was associated with the loss of mitochondrial CPT-II activity and alterations in the MMP, with decreases in liver CD3+ or CD4+ T cells and increased AFP levels. In the lipid accumulation microenvironment, mitochondrial CPT-II was inactivated, followed by aberrant activation of CD44+ or CD24+ LCSCs, as validated in MAFLD or hepatocellular carcinoma patient samples. In terms of mechanism, the biological process category focused mainly on the metabolic regulation of cells in response to external stimuli. The enriched molecular functions included protein binding, cell apoptosis, and cell proliferation. CONCLUSION CPT-II inactivity promotes the malignant progression of MAFLD via the loss of innate immune function and abnormal LCSC activation.
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Affiliation(s)
- Ling-Ling Wang
- Department of Immunology, Medical School, Nantong University, Nantong 226001, Jiangsu Province, China
| | - Yu-Ming Lu
- Department of Immunology, Medical School, Nantong University, Nantong 226001, Jiangsu Province, China
| | - Yi-Han Wang
- Department of Immunology, Medical School, Nantong University, Nantong 226001, Jiangsu Province, China
| | - Yi-Fan Wang
- Department of Immunology, Medical School, Nantong University, Nantong 226001, Jiangsu Province, China
| | - Rong-Fei Fang
- Department of Gastroenterology, The Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu Province, China
| | - Wen-Li Sai
- Research Center of Clinical Medicine, The Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu Province, China
| | - Deng-Fu Yao
- Research Center of Clinical Medicine, The Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu Province, China
| | - Min Yao
- Department of Immunology, Medical School, Nantong University, Nantong 226001, Jiangsu Province, China
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Cesarini L, Grignaffini F, Alisi A, Pastore A. Alterations in Glutathione Redox Homeostasis in Metabolic Dysfunction-Associated Fatty Liver Disease: A Systematic Review. Antioxidants (Basel) 2024; 13:1461. [PMID: 39765791 PMCID: PMC11672975 DOI: 10.3390/antiox13121461] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/22/2024] [Revised: 11/18/2024] [Accepted: 11/25/2024] [Indexed: 01/11/2025] Open
Abstract
Low molecular weight (LMW) thiols, particularly glutathione, play pathogenic roles in various multiorgan diseases. The liver is central for the production and systemic distribution of LMW thiols; thus, it is particularly susceptible to the imbalance of redox status that may determine increased oxidative stress and trigger the liver damage observed in metabolic dysfunction-associated steatotic liver disease (MASLD) models and humans. Indeed, increased LMW thiols at the cellular and extracellular levels may be associated with the severity of MASLD. Here, we present a systematic literature review of recent studies assessing the levels of LMW thiols in MASLD in in vivo and in vitro models and human subjects. Based on the PRISMA 2020 criteria, a search was conducted using PubMed and Scopus by applying inclusion/exclusion filters. The initial search returned 1012 documents, from which 165 eligible studies were selected, further described, and qualitatively analysed. Of these studies, most focused on animal and cellular models, while a minority used human fluids. The analysis of these studies revealed heterogeneity in the methods of sample processing and measurement of LMW thiol levels, which hinder cut-off values for diagnostic use. Standardisation of the analysis and measure of LMW thiol is necessary to facilitate future studies.
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Affiliation(s)
| | | | - Anna Alisi
- Research Unit of Genetics of Complex Phenotypes, Bambino Gesù Children’s Hospital, IRCCS, 00165 Rome, Italy; (L.C.); (F.G.); (A.P.)
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Song J, Peng D, Peng Y, Zhao G, Ren Y, Guo L, Ren L, Zhang X, Xie X, Zhang Y, Cao L, Li Y. The new pattern for dual NOTCH pathway involving nuclear transcription and mitochondrial regulation supports therapeutic mechanism of 4-butyl benzophenone derivatives against SIRS. Free Radic Biol Med 2024; 223:306-324. [PMID: 39134162 DOI: 10.1016/j.freeradbiomed.2024.07.036] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/12/2024] [Revised: 07/01/2024] [Accepted: 07/30/2024] [Indexed: 08/17/2024]
Abstract
The systemic inflammatory response syndrome (SIRS) represents a self-amplifying cascade of inflammatory reactions and pathophysiological states triggered by infectious or non-infectious factors. The identification of disease targets and differential proteins in the liver (the unique and important immune organ) of SIRS mice treated with the lead compound D1 was conducted using the Genecards database and proteomic analysis, respectively. Subsequently, NOTCH1 was identified as the potential hub target via an intersection analysis between the aforementioned differentially expressed proteins and disease targets. Based on our previous research on the structure-activity relationship, we designed and synthesized a series of SIRS-related derivatives, wherein butyl, halogen, and ester groups were incorporated into benzophenone, aiming at exploring the anti-inflammatory protective action from the perspective of macrophage polarization. Notably, these derivatives exhibited a direct binding capability to the O-glucosylation site (SER496) or its vicinities (such as SER492, VAL485) of NOTCH1 using docking, SPR, DARTS, and CETSA techniques. Mechanistically, derivative D6 exerted anti-inflammatory effects via the dual NOTCH pathway. Firstly, it could inhibit NOTCH1 nuclear transcriptional activity, attenuate the interaction between NICD and RBPJK, concurrently suppress NF-κB and NLRP3 inflammasome (NLRP3, ASC, and cleaved CASP1) activation, and promote NICD (NOTCH1 active fragments) ubiquitination metabolism (the nuclear transcriptional pathway). Secondly, it might possess the ability to increase PGC1α level, subsequently, enhance ATP and MMP levels, mitigate ROS production, increase mitochondrial numbers, and ameliorate mitochondrial inflammatory damage (the mitochondrial pathway). Importantly, the activator Jagged1 could effectively reverse the aforementioned effects, while the inhibitor DAPT exhibited a synergistic effect, suggesting that the nuclear transcriptional regulation and mitochondrial regulation were both in a NOTCH1-dependent manner. Subsequently, it effectively alleviated the inflammatory response and preserved organ function as evidenced by up-regulating M2-type macrophage-related anti-inflammatory cytokines (IL10, TGFβ, CD206, and ARG1) and down-regulating M1-type macrophage-related pro-inflammatory cytokines (NO, IL6, IL18, iNOS, TNFα, CD86, and IL1β). In a word, derivative D6 modulated macrophage polarization and effectively mitigated SIRS by targeting inhibition of the dual NOTCH pathway.
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Affiliation(s)
- Jiayu Song
- School of Pharmaceutical Science, Shanxi Medical University, Taiyuan 030001, PR China
| | - Dan Peng
- School of Pharmaceutical Science, Shanxi Medical University, Taiyuan 030001, PR China
| | - Yu Peng
- School of Pharmaceutical Science, Shanxi Medical University, Taiyuan 030001, PR China
| | - Guang Zhao
- School of Pharmaceutical Science, Shanxi Medical University, Taiyuan 030001, PR China
| | - Yuan Ren
- School of Pharmaceutical Science, Shanxi Medical University, Taiyuan 030001, PR China
| | - Lina Guo
- School of Pharmaceutical Science, Shanxi Medical University, Taiyuan 030001, PR China
| | - Luyao Ren
- School of Pharmaceutical Science, Shanxi Medical University, Taiyuan 030001, PR China
| | - Xiaohui Zhang
- School of Pharmaceutical Science, Shanxi Medical University, Taiyuan 030001, PR China
| | - Xiaoxia Xie
- School of Pharmaceutical Science, Shanxi Medical University, Taiyuan 030001, PR China
| | - Yajie Zhang
- School of Pharmaceutical Science, Shanxi Medical University, Taiyuan 030001, PR China
| | - Lingya Cao
- School of Pharmaceutical Science, Shanxi Medical University, Taiyuan 030001, PR China
| | - Yunlan Li
- School of Pharmaceutical Science, Shanxi Medical University, Taiyuan 030001, PR China; School of Public Health, Shaanxi University of Chinese Medicine, Xi'an 712046, PR China.
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6
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Tian C, Huang R, Xiang M. SIRT1: Harnessing multiple pathways to hinder NAFLD. Pharmacol Res 2024; 203:107155. [PMID: 38527697 DOI: 10.1016/j.phrs.2024.107155] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/16/2024] [Revised: 03/04/2024] [Accepted: 03/21/2024] [Indexed: 03/27/2024]
Abstract
Non-alcoholic fatty liver disease (NAFLD) encompasses hepatic steatosis, non-alcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and hepatocellular carcinoma. It is the primary cause of chronic liver disorders, with a high prevalence but no approved treatment. Therefore, it is indispensable to find a trustworthy therapy for NAFLD. Recently, mounting evidence illustrates that Sirtuin 1 (SIRT1) is strongly associated with NAFLD. SIRT1 activation or overexpression attenuate NAFLD, while SIRT1 deficiency aggravates NAFLD. Besides, an array of therapeutic agents, including natural compounds, synthetic compounds, traditional Chinese medicine formula, and stem cell transplantation, alleviates NALFD via SIRT1 activation or upregulation. Mechanically, SIRT1 alleviates NAFLD by reestablishing autophagy, enhancing mitochondrial function, suppressing oxidative stress, and coordinating lipid metabolism, as well as reducing hepatocyte apoptosis and inflammation. In this review, we introduced the structure and function of SIRT1 briefly, and summarized the effect of SIRT1 on NAFLD and its mechanism, along with the application of SIRT1 agonists in treating NAFLD.
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Affiliation(s)
- Cheng Tian
- Department of Pharmacology, School of Pharmacy, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China
| | - Rongrong Huang
- Department of Pharmacy, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China
| | - Ming Xiang
- Department of Pharmacology, School of Pharmacy, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
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Xu Y, Wang XC, Jiang W, Hu JN. Angelica sinensis polysaccharides modified selenium nanoparticles for effective prevention of acute liver injury. Int J Biol Macromol 2024; 263:130321. [PMID: 38382780 DOI: 10.1016/j.ijbiomac.2024.130321] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/16/2023] [Revised: 11/21/2023] [Accepted: 02/18/2024] [Indexed: 02/23/2024]
Abstract
As a global public health issue, the treatment of acute liver injury (ALI) is severely limited due to the lack of specific drugs. In order to address the challenges, innovative strategies for selenium nanoparticles (Se NPs) with excellent antioxidant properties have been actively developed to effectively prevent ALI. However, the functional activity of Se NPs is severely affected by poor stability and bioavailability. The aim of this work is to develop a stabilization system (ASP-Se NPs) for Angelica sinensis polysaccharides modified Se NPs. The results showed that ASP-Se NPs with smaller size (62.38 ± 2.96 nm) showed good stability, specific accumulation in liver and enhanced cell uptake, thus exerting strong antioxidant and anti-inflammatory functions. The results of in vivo experiments further confirmed that ASP-Se NPs effectively prevented CCl4-induced ALI by improving liver function, inhibiting oxidative stress and inflammatory response, and liver pathological damage. This work provides a new alternative method for effectively preventing ALI and improving liver function.
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Affiliation(s)
- Yu Xu
- SKL of Marine Food Processing & Safety Control, National Engineering Research Center of Seafood, Collaborative Innovation Center of Seafood Deep Processing, School of Food Science and Technology, Dalian Polytechnic University, Dalian 116034, China
| | - Xin-Chuang Wang
- SKL of Marine Food Processing & Safety Control, National Engineering Research Center of Seafood, Collaborative Innovation Center of Seafood Deep Processing, School of Food Science and Technology, Dalian Polytechnic University, Dalian 116034, China
| | - Wen Jiang
- SKL of Marine Food Processing & Safety Control, National Engineering Research Center of Seafood, Collaborative Innovation Center of Seafood Deep Processing, School of Food Science and Technology, Dalian Polytechnic University, Dalian 116034, China
| | - Jiang-Ning Hu
- SKL of Marine Food Processing & Safety Control, National Engineering Research Center of Seafood, Collaborative Innovation Center of Seafood Deep Processing, School of Food Science and Technology, Dalian Polytechnic University, Dalian 116034, China.
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Wang M, Zhao J, Chen J, Long T, Xu M, Luo T, Che Q, He Y, Xu D. The role of sirtuin1 in liver injury: molecular mechanisms and novel therapeutic target. PeerJ 2024; 12:e17094. [PMID: 38563003 PMCID: PMC10984179 DOI: 10.7717/peerj.17094] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/21/2023] [Accepted: 02/20/2024] [Indexed: 04/04/2024] Open
Abstract
Liver disease is a common and serious threat to human health. The progression of liver diseases is influenced by many physiologic processes, including oxidative stress, inflammation, bile acid metabolism, and autophagy. Various factors lead to the dysfunction of these processes and basing on the different pathogeny, pathology, clinical manifestation, and pathogenesis, liver diseases are grouped into different categories. Specifically, Sirtuin1 (SIRT1), a member of the sirtuin protein family, has been extensively studied in the context of liver injury in recent years and are confirmed the significant role in liver disease. SIRT1 has been found to play a critical role in regulating key processes in liver injury. Further, SIRT1 seems to cause divers outcomes in different types of liver diseases. Recent studies have showed some therapeutic strategies involving modulating SIRT1, which may bring a novel therapeutic target. To elucidate the mechanisms underlying the role of sirtuin1 in liver injury and its potentiality as a therapeutic target, this review outlines the key signaling pathways associated with sirtuin1 and liver injury, and discusses recent advances in therapeutic strategies targeting sirtuin1 in liver diseases.
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Affiliation(s)
- Mufei Wang
- Department of Medical Instrumental Analysis, Zunyi Medical University, Zunyi, Guizhou, China
- Department of Infectious Diseases, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou, China
| | - Juanjuan Zhao
- Department of Immunology, Zunyi Medical University, Zunyi, Guizhou, China
| | - Jiuxia Chen
- Department of Medical Instrumental Analysis, Zunyi Medical University, Zunyi, Guizhou, China
| | - Teng Long
- Department of Medical Instrumental Analysis, Zunyi Medical University, Zunyi, Guizhou, China
| | - Mengwei Xu
- Department of Medical Instrumental Analysis, Zunyi Medical University, Zunyi, Guizhou, China
| | - Tingting Luo
- Department of Medical Instrumental Analysis, Zunyi Medical University, Zunyi, Guizhou, China
| | - Qingya Che
- Department of Medical Instrumental Analysis, Zunyi Medical University, Zunyi, Guizhou, China
| | - Yihuai He
- Department of Infectious Diseases, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou, China
| | - Delin Xu
- Department of Medical Instrumental Analysis, Zunyi Medical University, Zunyi, Guizhou, China
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