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Here we delineate a novel selenium\u2010selenoprotein H (SELENOH)\u2010PPAR\u03b1 signaling axis that is critical for hepatic lipid homeostasis. We first uncovered a global impairment of selenoprotein translation as a key feature of metabolic dysfunction\u2010associated steatohepatitis (MASH) in human patients and mouse models. Both dietary selenium supplementation and genetically rescuing selenoprotein biosynthesis attenuated MASH pathology, establishing a causal link. Through a targeted screen, we pinpointed SELENOH as the key hepatoprotective selenoprotein governing hepatic fatty acid oxidation (FAO). Diverging from the canonical redox functions of selenoproteins, SELENOH operates as a scaffolding coactivator for the nuclear receptor PPAR\u03b1. SELENOH binds to ligand\u2010activated PPAR\u03b1 and orchestrates the assembly and chromatin recruitment of the PPAR\u03b1\u2010P300 transactivation complex to drive FAO gene expression. This nexus is disrupted in MASH livers due to SELENOH deficiency but is reconstituted by selenium supplementation. These findings altogether define selenium homeostasis as a fundamental regulator of nuclear receptor function and unveil promising therapeutic avenues for MASH.<\/jats:p>","DOI":"10.1002\/advs.202519563","type":"journal-article","created":{"date-parts":[[2026,2,8]],"date-time":"2026-02-08T18:07:09Z","timestamp":1770574029000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Selenoprotein H Functions as a PPAR\u03b1 Coactivator to Link Selenium Homeostasis to Hepatic Lipid Metabolism and Protect against Steatohepatitis"],"prefix":"10.1002","volume":"13","author":[{"given":"Yuwei","family":"Zhang","sequence":"first","affiliation":[{"name":"CAS Key Laboratory of Nutrition Metabolism and Food Safety Shanghai Institute of Nutrition and Health University of Chinese Academy of Sciences Chinese Academy of Sciences  P. R. 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