{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,10]],"date-time":"2026-07-10T10:50:51Z","timestamp":1783680651265,"version":"3.55.0"},"reference-count":31,"publisher":"Wiley","issue":"13","license":[{"start":{"date-parts":[[2025,7,3]],"date-time":"2025-07-03T00:00:00Z","timestamp":1751500800000},"content-version":"vor","delay-in-days":2,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2025,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>The aim of the present study was to explore the effect of the non\u2010steroidal anti\u2010inflammatory drugs (NSAID) aspirin on the progression of liver fibrosis and to elucidate its underlying mechanisms, with a specific focus on autophagy. In\u00a0vitro, the rat hepatic stellate cell line HSC\u2010T6 was activated using transforming growth factor\u2010\u03b21 (TGF\u2010\u03b21). Western blot and real\u2010time PCR analysis were employed to investigate the effect of aspirin on HSC\u2010T6 activation and its association with autophagy levels, including key autophagic markers. In\u00a0vivo study, liver fibrosis was induced in mice via long\u2010term thioacetamide (TAA) administration. The impact of aspirin on liver fibrosis and function was evaluated using Masson's Trichrome and Sirius Red staining to assess collagen deposition, complemented by serum biochemistry analysis. TGF\u2010\u03b21 treatment inhibited autophagic flux in activated HSC\u2010T6 cells, as evidenced by increased LC3II\/I and p62 expression. Notably, aspirin effectively attenuated fibrogenesis in these cells, with significantly lower expression levels of \u03b1\u2010SMA and collagen I compared to the TGF\u2010\u03b21\u2010treated control group. Concurrently, aspirin restored autophagy flux as indicated by decreased LC3\u2010II\/I and p62 levels, and the effect can be reversed by the autophagy inhibitor chloroquine (CQ). In\u00a0vivo, aspirin administration markedly attenuated liver fibrosis. Mechanistically, aspirin treatment enhanced autophagic flux, as demonstrated by the accumulation of autolysosomes observed in liver tissues via transmission electron microscopy (TEM). Our study demonstrates that aspirin inhibits liver fibrosis progression by inducing autophagy, highlighting its potential as a therapeutic strategy for liver fibrosis.<\/jats:p>","DOI":"10.1111\/jcmm.70696","type":"journal-article","created":{"date-parts":[[2025,7,4]],"date-time":"2025-07-04T00:30:22Z","timestamp":1751589022000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Aspirin Attenuates Liver Fibrosis via Autophagy Induction"],"prefix":"10.1111","volume":"29","author":[{"given":"Shenglan","family":"Wang","sequence":"first","affiliation":[{"name":"Division of Gastroenterology and Institute of Digestive Disease Tongji Hospital, Tongji University School of Medicine  Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mengxue","family":"Sun","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology and Institute of Digestive Disease Tongji Hospital, Tongji 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