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Obesity\u2010driven mechanisms, including adipose tissue dysfunction, insulin resistance and increased free fatty acid flux to the liver, promote ectopic lipid accumulation and lipotoxic injury. These processes trigger mitochondrial and endoplasmic reticulum stress, inflammation, immune activation and disturbances in the gut\u2013liver axis, driving disease progression from simple steatosis to metabolic dysfunction\u2013associated steatohepatitis, fibrosis and cirrhosis. MASLD is a highly heterogeneous condition, with differences in fat distribution, body composition and genetic susceptibility giving rise to distinct clinical phenotypes, including lean and non\u2010lean MASLD, which have important implications for disease risk, progression and therapeutic response. Clinical outcomes are determined primarily by fibrosis stage, which represents the strongest predictor of liver\u2010related and all\u2010cause mortality, underscoring the importance of early disease recognition and risk stratification. Therapeutic strategies, therefore, increasingly target upstream metabolic drivers rather than hepatic steatosis alone. Lifestyle interventions remain foundational but are often limited by challenges in long\u2010term adherence. Pharmacologic therapies, particularly incretin\u2010based agents such as glucagon\u2010like peptide\u20101 receptor agonists and dual incretin agonists, as well as bariatric and endoscopic metabolic procedures, have demonstrated substantial metabolic and hepatic benefits. Recognition of disease heterogeneity supports phenotype\u2010guided approaches that integrate metabolic risk, adiposity, body composition and fibrosis assessment to personalise treatment strategies and improve long\u2010term outcomes across the MASLD spectrum.<\/jats:p>","DOI":"10.1111\/dom.70659","type":"journal-article","created":{"date-parts":[[2026,4,6]],"date-time":"2026-04-06T08:07:29Z","timestamp":1775462849000},"page":"19-30","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":25,"title":["Obesity and Metabolic Dysfunction\u2010Associated Steatotic Liver Disease (\n                    <scp>MASLD<\/scp>\n                    ): A Literature Review on Pathophysiology and Treatment"],"prefix":"10.1111","volume":"28","author":[{"given":"Michael","family":"Romanos","sequence":"first","affiliation":[{"name":"Precision Medicine for Obesity Program, Division of Gastroenterology and Hepatology Department of Medicine, Mayo Clinic  Rochester Minnesota USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Juan M.","family":"Garcia Cordova","sequence":"additional","affiliation":[{"name":"Precision Medicine for Obesity Program, Division of Gastroenterology and Hepatology Department of Medicine, Mayo Clinic  Rochester Minnesota USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jose","family":"Villamarin","sequence":"additional","affiliation":[{"name":"Precision Medicine for Obesity Program, Division of Gastroenterology and Hepatology Department of Medicine, Mayo Clinic  Rochester Minnesota USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Juan D.","family":"Pazmino Zurita","sequence":"additional","affiliation":[{"name":"Precision Medicine for Obesity Program, Division of Gastroenterology and Hepatology Department of Medicine, Mayo Clinic  Rochester Minnesota USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2286-489X","authenticated-orcid":false,"given":"Andres","family":"Acosta","sequence":"additional","affiliation":[{"name":"Precision Medicine for Obesity Program, Division of Gastroenterology and Hepatology Department of Medicine, Mayo Clinic  Rochester Minnesota USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,4,6]]},"reference":[{"issue":"7","key":"e_1_2_8_2_1","doi-asserted-by":"crossref","first-page":"715","DOI":"10.1111\/obr.12551","article-title":"Obesity: A Chronic Relapsing Progressive Disease Process. 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