{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T04:49:16Z","timestamp":1791434956382,"version":"4.3.3"},"reference-count":69,"publisher":"Wiley","license":[{"start":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T00:00:00Z","timestamp":1791331200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T00:00:00Z","timestamp":1791331200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Phytotherapy Research"],"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Metabolic dysfunction\u2010associated fatty liver disease (MAFLD) lacks effective pharmacological therapies and is strongly associated with excessive fructose consumption. Ferroptosis and autophagy dysregulation are increasingly recognized as key drivers of MAFLD progression. Epigallocatechin\u20103\u2010gallate (EGCG) exerts hepatoprotective effects. However, whether it regulates SIRT5\u2010mediated ferroptosis and autophagy remains unclear. This study was aimed at investigating whether EGCG ameliorates fructose\u2010induced MAFLD by regulating ferroptosis and autophagy via SIRT5. A fructose\u2010induced MAFLD mouse model and fructose\u2010treated HepG2 cells were established, and EGCG intervention was performed with or without SIRT5 knockdown. Hepatic steatosis, inflammation, ferroptosis\u2010 and autophagy\u2010related markers were evaluated by biochemical assays, histological analysis, RT\u2010qPCR, and western blotting analysis. Molecular docking was used to assess the interaction between EGCG and SIRT5. EGCG significantly mitigated hepatic lipid accumulation and inflammation in fructose\u2010induced MAFLD models. It restored SIRT5 expression, alleviated iron overload and oxidative stress, rescued GPX4 and FTH1 expression, and downregulated FTL and COX2 levels. EGCG also improved autophagy, as reflected by an elevated LC3\u2010II\/LC3\u2010I ratio and LAMP2 expression, together with reduced SQSTM1\/p62 accumulation. Importantly, SIRT5 knockdown abolished these protective effects, suggesting a SIRT5\u2010dependent mechanism. Molecular docking analysis further verified a robust binding affinity between EGCG and SIRT5. Collectively, our results demonstrate that EGCG ameliorates fructose\u2010induced MAFLD by modulating ferroptosis and autophagy through SIRT5 upregulation, highlighting SIRT5 as a potential therapeutic target and supporting EGCG as a promising intervention for MAFLD.<\/jats:p>","DOI":"10.1002\/ptr.70477","type":"journal-article","created":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T03:51:58Z","timestamp":1791431518000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Protective Effect of Epigallocatechin\u20103\u2010Gallate Against Fructose\u2010Induced Metabolic Associated Fatty Liver Disease in Mice by Regulating Ferroptosis and Autophagy via\n                    <scp>SIRT5<\/scp>"],"prefix":"10.1002","author":[{"given":"Puyu","family":"Zhang","sequence":"first","affiliation":[{"name":"Key Laboratory of Precision Medical Research on Major Chronic Disease, Shengjing Hospital of China Medical University  Shenyang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cuiping","family":"Hou","sequence":"additional","affiliation":[{"name":"Key Laboratory of Precision Medical Research on Major Chronic Disease, Shengjing Hospital of China Medical University  Shenyang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiayi","family":"Liu","sequence":"additional","affiliation":[{"name":"Key Laboratory of Precision Medical Research on Major Chronic Disease, Shengjing Hospital of China Medical University  Shenyang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bosheng","family":"Wang","sequence":"additional","affiliation":[{"name":"Key Laboratory of Precision Medical Research on Major Chronic Disease, Shengjing Hospital of China Medical University  Shenyang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wenqi","family":"Liu","sequence":"additional","affiliation":[{"name":"Key Laboratory of Precision Medical Research on Major Chronic Disease, Shengjing Hospital of China Medical University  Shenyang China"},{"name":"Department of Clinical Epidemiology Shengjing Hospital of China Medical University  Shenyang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xin","family":"Yang","sequence":"additional","affiliation":[{"name":"Key Laboratory of Precision Medical Research on Major Chronic Disease, Shengjing Hospital of China Medical University  Shenyang China"},{"name":"Department of Clinical Epidemiology Shengjing Hospital of China Medical University  Shenyang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yubing","family":"Kang","sequence":"additional","affiliation":[{"name":"Key Laboratory of Precision Medical Research on Major Chronic Disease, Shengjing Hospital of China Medical University  Shenyang China"},{"name":"Department of Clinical Epidemiology Shengjing Hospital of China Medical University  Shenyang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zequn","family":"Liu","sequence":"additional","affiliation":[{"name":"Key Laboratory of Precision Medical Research on Major Chronic Disease, Shengjing Hospital of China Medical University  Shenyang China"},{"name":"Department of Clinical Epidemiology Shengjing Hospital of China Medical University  Shenyang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yalin","family":"Zhang","sequence":"additional","affiliation":[{"name":"Key Laboratory of Precision Medical Research on Major Chronic Disease, Shengjing Hospital of China Medical University  Shenyang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhuxi","family":"Liu","sequence":"additional","affiliation":[{"name":"Key Laboratory of Precision Medical Research on Major Chronic Disease, Shengjing Hospital of China Medical University  Shenyang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuhong","family":"Zhao","sequence":"additional","affiliation":[{"name":"Key Laboratory of Precision Medical Research on Major Chronic Disease, Shengjing Hospital of China Medical University  Shenyang China"},{"name":"Department of Clinical Epidemiology Shengjing Hospital of China Medical University  Shenyang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0004-0451","authenticated-orcid":false,"given":"Lu","family":"Zhao","sequence":"additional","affiliation":[{"name":"Key Laboratory of Precision Medical Research on Major Chronic Disease, Shengjing Hospital of China Medical University  Shenyang China"},{"name":"Department of Clinical Epidemiology Shengjing Hospital of China Medical University  Shenyang China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,10,7]]},"reference":[{"key":"e_1_2_12_2_1","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1080\/15548627.2026.2711593","article-title":"Molecular Switches of Sqstm1: The Impact of Post\u2010Translational Modifications on Autophagy and Neurodegeneration","author":"Abrar F.","year":"2026","journal-title":"Autophagy"},{"issue":"1","key":"e_1_2_12_3_1","doi-asserted-by":"crossref","first-page":"73","DOI":"10.1186\/s43556-024-00240-9","article-title":"Epigallocatechin\u20103\u2010Gallate Therapeutic Potential in Human Diseases: Molecular Mechanisms and Clinical Studies","volume":"5","author":"Alam M.","year":"2024","journal-title":"Molecular Biomedicine"},{"issue":"5","key":"e_1_2_12_4_1","doi-asserted-by":"crossref","first-page":"440","DOI":"10.3390\/antiox9050440","article-title":"Bioavailability of Epigallocatechin Gallate Administered With Different Nutritional 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