{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T19:52:34Z","timestamp":1792785154385,"version":"4.5.0"},"reference-count":262,"publisher":"Georg Thieme Verlag KG","issue":"02","funder":[{"name":"National Institute of Diabetes and Digestive and Kidney Diseases","award":["DK114091, DK124510"],"award-info":[{"award-number":["DK114091, DK124510"]}],"id":[{"id":"https:\/\/ror.org\/00adh9b73","id-type":"ROR","asserted-by":"crossref"}]},{"name":"National Heart, Lung, and Blood Institute","award":["HL153532-01A1"],"award-info":[{"award-number":["HL153532-01A1"]}],"id":[{"id":"https:\/\/ror.org\/012pb6c26","id-type":"ROR","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Semin Liver Dis"],"published-print":{"date-parts":[[2026,6]]},"abstract":"<jats:p>Hyperuricemia and metabolic dysfunction\u2013associated steatotic liver disease share overlapping risk factors, yet the mechanistic contribution of uric acid remains unclear. Generation of uric acid occurs exclusively by xanthine oxidoreductase, a process intrinsically linked to electron transfer and oxidant generation, a relationship that can be viewed through electron accounting. This biochemical coupling makes it difficult to determine whether elevated uric acid drives pathology or reflects broader changes in increased redox\/oxidative stress. This review highlights mechanisms of uric acid production, its dual antioxidant and pro-oxidant effects, and regulation of urate transporters. We then discuss how western dietary patterns, adiposity, and insulin resistance reshape uric acid homeostasis and intersect with pathways that promote steatosis, inflammation, and fibrogenesis. In conclusion, by framing uric acid within a liver-centered redox perspective, we consider whether elevated uric acid functions as a biomarker of metabolic stress, a contributor to disease progression, and a potential therapeutic target in metabolic dysfunction\u2013associated steatotic liver disease.<\/jats:p>","DOI":"10.1055\/a-2926-5268","type":"journal-article","created":{"date-parts":[[2026,8,21]],"date-time":"2026-08-21T23:35:56Z","timestamp":1787355356000},"page":"116-134","source":"Crossref","is-referenced-by-count":0,"title":["Elevated Uric Acid and Metabolic Dysfunction\u2014Associated Steatotic Liver Disease Progression: Where There's Smoke, is There Fire?"],"prefix":"10.1055","volume":"46","author":[{"given":"Eric E.","family":"Kelley","sequence":"additional","affiliation":[{"name":"West Virginia University School of Medicine, West Virginia, United States","place":["Morgantown"],"department":["Department of Physiology, Pharmacology and Toxicology"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9514-2180","authenticated-orcid":false,"given":"Owen M.","family":"Woodward","sequence":"additional","affiliation":[{"name":"University of Maryland School of Medicine, Maryland, United States","place":["Baltimore"],"department":["Departments of Physiology and Medicine"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1950-3033","authenticated-orcid":false,"given":"Nicholas K.H.","family":"Khoo","sequence":"additional","affiliation":[{"name":"University of Pittsburgh, Organ Pathobiology and Therapeutics Institute, Pennsylvania, United States","place":["Pittsburgh"],"department":["Department of Pharmacology and Chemical Biology"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"194","published-online":{"date-parts":[[2026,8,21]]},"reference":[{"issue":"13","key":"ref1","doi-asserted-by":"crossref","first-page":"8370","DOI":"10.1074\/jbc.272.13.8370","article-title":"The reaction of reduced xanthine dehydrogenase with molecular oxygen. 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