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Cellular senescence in liver fibrosis: Implications for age-related chronic liver diseases
Wanvisa Udomsinprasert1, Abhasnee Sobhonslidsuk2, Jiraphun Jittikoon1
1Department of Biochemistry, Faculty of Pharmacy, Mahidol University, Bangkok, Thailand.
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.
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