Autophagy and senescence: the molecular mechanisms and implications in liver diseases
Open accessAbstract
The liver is the primary organ accountable for complex physiological functions, including lipid metabolism, toxic chemical degradation, bile acid synthesis, and glucose metabolism. Liver function homeostasis is essential for the stability of bodily functions and is involved in the complex regulation of the balance between cell proliferation and cell death. Cell proliferation-halting mechanisms, including autophagy and senescence, are implicated in the development of several liver diseases, such as cholestasis, viral hepatitis, nonalcoholic fatty liver disease, liver fibrosis, and hepatocellular carcinoma. Among various cell death mechanisms, autophagy is a highly conserved and self-degradative cellular process that recycles damaged organelles, cellular debris, and proteins. This process also provides the substrate for further metabolism. A defect in the autophagy machinery can lead to premature diseases, accelerated aging, inflammatory state, tumorigenesis, and cellular senescence. Senescence, another cell death type, is an active player in eliminating premalignant cells. At the same time, senescent cells can affect the function of neighboring cells by secreting the senescence-associated secretory phenotype and induce paracrine senescence. Autophagy can promote and delay cellular senescence under different contexts. This review decodes the roles of autophagy and senescence in multiple liver diseases to achieve a better understanding of the regulatory mechanisms and implications of autophagy and senescence in various liver diseases.
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Senescence and autophagy differential regulation is associated with liver fibrosis and cancer.
“Senescence and autophagy differential regulation is associated with liver fibrosis and cancer [34].”
From Mechanical stiffness orchestrates distinct regulation of <scp>MRTFs</scp> and <scp>YAP</scp> / <scp>TAZ</scp> transcriptional cofactors in hepatocytes (2026) · cites this paper as [34]
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Cited by
Sorted by citations
Torres‐Ortiz, B. S., Pérez‐Calixto, D., Carretero‐Ortega, J., Guzman‐López, A. G., Pinto‐Dueñas, D. C., Hernández‐Juárez, M., Jiménez‐Escobar, A., Rodríguez‐Hernández, A., Díaz‐Bello, B., Serna‐Márquez, N., et al. (2026) · The FEBS Journal · doi:10.1111/febs.70570
- Authors
- Li, Q., Lin, Y., Liang, G., Xiao, N., Zhang, H., Yang, X., Yang, J., & Liu, A.
- Affiliations
- Experimental Medicine Center, Tongji Hospital, Tongji Medical College, Huazhong University of Sciences and Technology, Wuhan 430100, China
- Tongji Hospital (CN)
- Corresponding author
- Liu, Anding
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2023-11-28
- Volume
- 24
- Issue
- 23
- Pages
- 16880
- ISSN
- 1422-0067 (ISSN-L)
- PMC
- PMC10706096
- OpenAlex
- W4389080766
- Cited by
- 43
- References
- 26
- Citations by year
- 2026: 10 · 2025: 19 · 2024: 14
- FWCI
- 1.68
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- International Journal of Molecular Sciences (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- the National Natural Science Fund of China (NSFC) (82071590, 82271596)
- Topics
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Keywords
- autophagy, cellular senescence, liver disease, senescence-associated secretory phenotype, paracrine senescence, hepatocellular carcinoma, non-alcoholic fatty liver disease, liver fibrosis, cholestasis, viral hepatitis, cell death, liver homeostasis
- MeSH terms
- Aging, Autophagy, Humans, Cellular Senescence, Non-alcoholic Fatty Liver Disease
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