ArticleCell biology and toxicology2023
Induction of Sestrin2 by pterostilbene suppresses ethanol-triggered hepatocyte senescence by degrading CCN1 via p62-dependent selective autophagy.
Article in Cell biology and toxicology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- The Potential of Polyphenols in Modulating the Cellular Senescence Process: Implications and Mechanism of Action.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Mechanism and role of nuclear laminin B1 in cell senescence and malignant tumors.Cell death discovery · 2024Review
- Article
- ZNF281 drives hepatocyte senescence in alcoholic liver disease by reducing HK2-stabilized PINK1/Parkin-mediated mitophagy.Cell proliferation · 2023Article
- Sestrin2: multifaceted functions, molecular basis, and its implications in liver diseases.Cell death & disease · 2023Review
- Natural-Product-Mediated Autophagy in the Treatment of Various Liver Diseases.International journal of molecular sciences · 2022Review
- CCN1/Integrin αNutrients · 2022Article
- Nutritional components as mitigators of cellular senescence in organismal aging: a comprehensive review.Food science and biotechnology · 2022Review
- Forward single-cell sequencing into clinical application: Understanding of ageing and rejuvenation from clinical observation to single-cell solution.Clinical and translational medicine · 2022Article
- Article
- Curcumol Suppresses CCF-Mediated Hepatocyte Senescence Through Blocking LC3B-Lamin B1 Interaction in Alcoholic Fatty Liver Disease.Frontiers in pharmacology · 2022Article
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Authors and funding
7 authors at 3 institutions in 1 country.
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Abstract
Hepatocyte senescence is a key event participating in the progression of alcoholic liver disease. Autophagy is a critical biological process that controls cell fates by affecting cell behaviors like senescence. Pterostilbene is a natural compound with hepatoprotective potential; however, its implication for alcoholic liver disease was not understood. This study was aimed to investigate the therapeutic effect of pterostilbene on alcoholic liver disease and elucidate the potential mechanism. Our results showed that pterostilbene alleviated ethanol-triggered hepatocyte damage and senescence. Intriguingly, pterostilbene decreased the protein abundance of cellular communication network factor 1 (CCN1) in ethanol-exposed hepatocytes, which was essential for pterostilbene to execute its anti-senescent function. In vivo studies verified the anti-senescent effect of pterostilbene on hepatocytes of alcohol-intoxicated mice. Pterostilbene also relieved senescence-associated secretory phenotype (SASP), redox imbalance, and steatosis by suppressing hepatic CCN1 expression. Mechanistically, pterostilbene-forced CCN1 reduction was dependent on posttranscriptional regulation via autophagy machinery but not transcriptional regulation. To be specific, pterostilbene restored autophagic flux in damaged hepatocytes and activated p62-mediated selective autophagy to recognize and lead CCN1 to autolysosomes for degradation. The protein abundance of Sestrin2 (SESN2), a core upstream modulator of autophagy pathway, was decreased in ethanol-administrated hepatocytes but rescued by co-treatment with pterostilbene. Induction of SESN2 protein by pterostilbene rescued ethanol-triggered autophagic dysfunction in hepatocytes, which then reduced senescence-associated markers, postponed hepatocyte senescence, and relieved alcohol-caused liver injury and inflammation. In conclusion, this work discovered a novel compound pterostilbene with therapeutic implications for alcoholic liver disease and uncover its underlying mechanism.
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