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REVIEW article

Front. Pharmacol.

Sec. Gastrointestinal and Hepatic Pharmacology

Modulation of STAT6 signaling for hepatoprotection

Provisionally accepted
Emmanuel  SOMMEmmanuel SOMM*Mahdi  RahmanMahdi RahmanIldiko  SzantoIldiko SzantoKarim  GarianiKarim GarianiFrancois  R JornayvazFrancois R Jornayvaz
  • Service d'endocrinologie, diabétologie, nutrition et éducation thérapeutique, Hôpitaux universitaires de Genève (HUG), Geneva, Switzerland

The final, formatted version of the article will be published soon.

Signal transducer and activator of transcription (STAT) proteins are a family of seven transcription factors mediating various biological processes. STAT6 is classically known to regulate immune cell biology by transmitting signals from interleukin (IL)-4 and IL-13 into transcriptional activation of genes driving type 2 immunity. In orchestrating T helper lymphocytes and macrophages polarization, STAT6 plays a central role in the regulation of both cellular and humoral immunities. Several pathologies, including inflammatory disorders, autoimmune/allergic diseases, metabolic syndrome as well as cancer, are associated with a dysregulation of type 2 immunity related to inadequate expression and/or activity of STAT6. In the present review, following a brief introduction of STAT6 biology, we summarize the immunologic and physiological roles of STAT6 in the context of liver integrity as well as the potential roles of STAT6-mediated pathways in both hepatoprotection and liver pathophysiological mechanisms.

Keywords: STAT6, Ischemia - reperfusion, Acute liver damage, MASLD, MASH, Fibrosis, HCC, immune polarization

Received: 03 Jul 2025; Accepted: 31 Oct 2025.

Copyright: © 2025 SOMM, Rahman, Szanto, Gariani and Jornayvaz. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Emmanuel SOMM, emmanuel.somm@unige.ch

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