REVIEW article
Front. Immunol.
Sec. Autoimmune and Autoinflammatory Disorders : Autoimmune Disorders
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1639196
ECM Remodeling in Hypothyroidism-Associated MAFLD: Mechanisms, Clinical Relevance, and Therapeutic Targets
Provisionally accepted
- 1Changchun University of Chinese Medicine, Changchun, China
- 2Affiliated Hospital to Changchun University of Chinese Medicine, Changchun, China
- 3Jilin Province People's Hospital, Changchun, China
- 4Shandong University of Traditional Chinese Medicine, Jinan, China
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Metabolic dysfunction–associated fatty liver disease (MAFLD) is a major chronic liver disease increasingly linked to endocrine and immunometabolic dysregulation. Hypothyroidism, both overt and subclinical, has emerged as a significant endocrine risk factor for MAFLD. Extracellular matrix (ECM) remodeling, a hallmark of fibrosis, represents a crucial but underexplored mediator in this process. This review highlights how altered thyroid hormone (TH) and thyroid-stimulating hormone (TSH) signaling promote ECM remodeling through metabolic, inflammatory, and fibrogenic pathways, with emphasis on hepatic stellate cell (HSC) activation and immune reshaping. We further summarize ECM-derived biomarkers and emerging therapeutic strategies, including THRβ agonists and ECM-targeted approaches.
Keywords: Hypothyroidism, MAFLD, ECM remodeling, HSC, TH signaling , Liverfibrosis
Received: 01 Jun 2025; Accepted: 17 Sep 2025.
Copyright: © 2025 Wang, Zhao, Zhao, Duan, Zhang and Yu. 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:
Jinyue Zhao, 97394541@qq.com
Yongjiang Yu, 345532112@qq.com
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