{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T21:51:39Z","timestamp":1788299499144,"version":"build-2803163510"},"reference-count":70,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,8,11]],"date-time":"2026-08-11T00:00:00Z","timestamp":1786406400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Pharmacol."],"abstract":"<jats:p>Obeticholic acid (OCA) is not approved for metabolic dysfunction-associated steatohepatitis (MASH), and the United States development pathway for its use in precirrhotic NASH ended after regulatory non-approval. The compound is still useful scientifically, because no other farnesoid X receptor (FXR) agonist has produced a comparable human dataset in steatohepatitis. A frequent interpretive problem is that histological benefit, low-density lipoprotein cholesterol (LDL-C) elevation, pruritus and possible liver-intrinsic injury are compressed into one FXR activation continuum. This hypothesis-driven narrative article argues for a narrower reading. OCA is treated here as an index scaffold that separates clinical response, systemic lipid risk, tolerability and candidate liver-intrinsic sterol-stress biology into distinct evidence layers. We first place OCA in the current MASLD\/MASH therapeutic setting, then outline hepatic and intestinal FXR pharmacology relevant to the model. Human OCA data, cross-scaffold observations from non-bile acid FXR agonists, and mechanistic work on FATP5\/SLC27A5, cholesterol stress and ACOX1 are then reassessed. Within the proposed model, FATP5 is a putative OCA-linked substrate-entry node supported mainly by preclinical and humanized-transporter work. Cholesterol retention, free-cholesterol burden, cholesterol crystals, macrophage crown-like structures, IL-1beta signaling and hepatic stellate-cell activation are better handled as a candidate sterol-stress liability branch. ACOX1 is interpreted as a context-dependent modifier, not as a validated therapeutic target. The model is not a class-wide claim for all FXR agonists. It should be tested, and if necessary rejected, using matched FXR target engagement, paired human tissue and human multicellular systems.<\/jats:p>","DOI":"10.3389\/fphar.2026.1879097","type":"journal-article","created":{"date-parts":[[2026,8,11]],"date-time":"2026-08-11T07:44:04Z","timestamp":1786434244000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["Obeticholic acid as an index farnesoid X receptor scaffold in metabolic dysfunction-associated steatohepatitis: a testable model for efficacy-liability separation and biomarker interpretation"],"prefix":"10.3389","volume":"17","author":[{"given":"Jinghong","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Gastroenterology, The First Affiliated Hospital of Jinan University","place":["Guangzhou, Guangdong, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaojuan","family":"Wu","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology, Ganzhou Hospital-Nanfang Hospital, Southern Medical University (Ganzhou People\u2019s Hospital)","place":["Ganzhou, Jiangxi, China"]},{"name":"Ganzhou Key Laboratory of Gastroenterology, The Affiliated Ganzhou Hospital of Nanchang University","place":["Ganzhou, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,8,11]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"1317","DOI":"10.1016\/j.jhep.2023.07.034","article-title":"FXR agonists in NASH treatment","volume":"79","author":"Adorini","year":"2023","journal-title":"J. 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