Publication: Cellular senescence in liver fibrosis: Implications for age-related chronic liver diseases
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Issued Date
2021-01-01
Resource Type
ISSN
17447631
14728222
14728222
Other identifier(s)
2-s2.0-85117592725
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Mahidol University
Rights Holder(s)
SCOPUS
Bibliographic Citation
Expert Opinion on Therapeutic Targets. Vol.25, No.9 (2021), 799-813
Suggested Citation
Wanvisa Udomsinprasert, Abhasnee Sobhonslidsuk, Jiraphun Jittikoon, Sittisak Honsawek, Usa Chaikledkaew Cellular senescence in liver fibrosis: Implications for age-related chronic liver diseases. Expert Opinion on Therapeutic Targets. Vol.25, No.9 (2021), 799-813. doi:10.1080/14728222.2021.1992385 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/76328
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Title
Cellular senescence in liver fibrosis: Implications for age-related chronic liver diseases
Abstract
Introduction: New insights indicate a causative link between cellular senescence and liver fibrosis. Senescent hepatic stellate cells (HSCs) facilitate fibrosis resolution, while senescence in hepatocytes and cholangiocytes acts as a potent mechanism driving liver fibrogenesis. In many clinical studies, telomeres and mitochondrial DNA contents, which are both aging biomarkers, were reportedly associated with a degree of liver fibrosis in patients with chronic liver diseases (CLDs); this highlights their potential as biomarkers for liver fibrogenesis. A deeper understanding of mechanisms underlying multi-step progression of senescence may yield new therapeutic strategies for age-related chronic liver pathologies. Areas covered: This review examines the recent findings from preclinical and clinical studies on mechanisms of senescence in liver fibrogenesis and its involvement in liver fibrosis. A comprehensive literature search in electronic databases consisting of PubMed and Scopus from inception to 31 August 2021 was performed. Expert opinion: Cellular senescence has diagnostic, prognostic, and therapeutic potential in progressive liver complications, especially liver fibrosis. Stimulating or reinforcing the immune response against senescent cells may be a promising and forthright biotherapeutic strategy. This approach will need a deeper understanding of the immune system’s ability to eliminate senescent cells and the molecular and cellular mechanisms underlying this process.