We are analyzing https://link.springer.com/article/10.1007/s10565-021-09635-8.

Title:
Induction of Sestrin2 by pterostilbene suppresses ethanol-triggered hepatocyte senescence by degrading CCN1 via p62-dependent selective autophagy | Cell Biology and Toxicology
Description:
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. Graphical abstract
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Keywords {🔍}

article, pubmed, google, scholar, cas, pterostilbene, senescence, autophagy, liver, hepatocytes, cell, wang, protein, data, chen, hepatocyte, disease, lead, zhang, analysis, ccn, zhou, china, central, equal, jiang, alcoholic, versus, abundance, cellular, hepatic, injury, cells, huang, shao, zheng, nantong, sestrin, jin, steatosis, access, high, vehicle, expressed, privacy, cookies, content, information, ethanoltriggered, factor,

Topics {✒️}

acetaminophen-induced liver injury month download article/chapter ethanol-induced hepatocyte necroptosis sa-β-gal staining alcohol-induced hepatocyte necroptosis obesity-related liver steatosis senescence-induced-functional alterations phosphorylation-induced e2f release p62-dependent selective autophagy alcoholic liver disease elicited endothelium-dependent relaxations oxidative stress-induced senescence pterostilbene-forced ccn1 reduction key event participating article cell biology postponed hepatocyte senescence full article pdf senescence explains age hepatic stellate cells privacy choices/manage cookies cell death dis related subjects autophagy-dependent manner nrf2 knockdown attenuates p62 protein abundance driven senescence slows cellular senescence exp biol med inhibit hepatic steatosis ethanol-exposed hepatocytes ethanol-administrated hepatocytes conditions privacy policy hepatic fibrosis code availability curr med chem induce lipocyte phenotype jak2/stat3 signaling high resolution image β-galactosidase sasp controls cell fates affecting cell behaviors additional information publisher liver steatosis nrf2-dependent mechanism article jiang european economic area critical biological process core upstream modulator mir-194/fxr axis enhanced anticancer therapeutics

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