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Further, patients with severe liver disease experience muscle weakness and fatigue. Hypoxia\u2010inducible factor 2\u03b1 (HIF2\u03b1) accumulates in the livers of MASLD patients. Here we sought to understand the role of hepatic HIF2\u03b1 in mediating hepatic and extra\u2010hepatic features of MASLD. Using an obese mouse model of MASLD, we investigated the impact of hepatocyte\u2010specific HIF2\u03b1 deletion (hHIF2\u03b1\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    ) on hepatic, cardiac and skeletal muscle metabolism, and cardiac function. Over 28\u2009weeks, mice were exposed to a high\u2010fat, high\u2010fructose, high\u2010cholesterol (GAN) diet, which induced obesity, hepatic steatosis, fibrosis and inflammation. hHIF2\u03b1\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    was associated with greater hepatic NADH\u2010supported mitochondrial respiration, higher sphingomyelin levels and protection against MASLD induced hyperinsulinaemia, but not against hepatic manifestations of MASLD. Instead, in the hearts of GAN\u2010fed mice, hHIF2\u03b1\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    caused diacylglycerol and long\u2010chain acyl\u2010carnitine accumulation and exacerbated diet\u2010induced ceramide accumulation. Langendorff\u2010perfused hearts from hHIF2\u03b1\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice showed systolic and diastolic dysfunction, including 24% lower left ventricular developed pressure and 34% lower maximal rate of relaxation (dP\/dt\n                    <jats:sub>min<\/jats:sub>\n                    ). However, isolated hearts from hHIF2\u03b1\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice were protected against MASLD\u2010associated sympathetic dominance, determined using autonomic receptor agonist stimulation. Both GAN\u2010feeding and hHIF2\u03b1\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    were associated with lower lean mass (14% and 5.4% lower than respective controls), whilst hHIF2\u03b1\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    enhanced OXPHOS\u2010associated protein levels in gastrocnemius muscle. Overall, hHIF2\u03b1\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    resulted in detrimental extra\u2010hepatic effects, including myocardial lipid accumulation, impaired cardiac function, and loss of whole\u2010body lean mass, thereby worsening the systemic presentation of MASLD\u2010associated pathological features.\n                  <\/jats:p>","DOI":"10.1002\/cph4.70283","type":"journal-article","created":{"date-parts":[[2026,10,10]],"date-time":"2026-10-10T03:27:51Z","timestamp":1791602871000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Hepatic\n                    <scp>HIF2\u03b1<\/scp>\n                    Modulates Extra\u2010Hepatic Disease\u2010Associated Phenotypes During Metabolic Dysfunction\u2010Associated Steatotic Liver Disease"],"prefix":"10.1002","volume":"16","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8350-2142","authenticated-orcid":false,"given":"Lorenz M. 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