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REVIEW article

Front. Endocrinol.

Sec. Diabetes: Molecular Mechanisms

Volume 16 - 2025 | doi: 10.3389/fendo.2025.1642436

This article is part of the Research TopicMolecular Insights into Fatty Liver Disease: Pathogenesis, Progression, and Therapeutic StrategiesView all 3 articles

Advancements in the understanding of mechanisms of the IL-6 family in relation to metabolic-associated fatty liver disease

Provisionally accepted
Jiale  LiuJiale Liu1Tao  WangTao Wang1Fuyuan  YangFuyuan Yang1*Ciren  PubuCiren Pubu2*
  • 1School of Basic Medicine, Yangtze University Health Science Center, Jingzhou, Hubei, China., Jingzhou, Hubei, China., China
  • 2Shannan Maternal and Child Health Hospital, Naidong District, Shannan, China, 山南市, China

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

As lifestyle patterns change, the rates of type 2 diabetes and obesity are increasing together, leading to an increase in metabolic-associated fatty liver disease (MAFLD), now recognized as the most frequently occurring liver disease globally. MAFLD presents a significant threat to public health and imposes a substantial socioeconomic burden. This condition encompasses a spectrum of hepatic manifestations, beginning with excessive fat accumulation and hepatic steatosis, and possibly progressing to non-alcoholic steatohepatitis (NASH), liver fibrosis, cirrhosis, and liver cancer. The pathogenesis of MAFLD is intricately linked to lipid accumulation, oxidative stress, and lipotoxicity.Notably, the interleukin-6 (IL-6) cytokine family has a complex role in the onset and development of MAFLD, primarily through the modulation of lipid metabolism, insulin resistance, inflammatory responses, and liver fibrosis. This review investigates how the IL-6 family affects the progression of MAFLD and considers the possibility of targeting the IL-6 family as a future therapeutic approach for MAFLD in future clinical applications.

Keywords: IL-6 family, metabolic-associated fatty liver disease, Lipid Metabolism, Insulin Resistance, Inflammation

Received: 09 Jun 2025; Accepted: 22 Aug 2025.

Copyright: © 2025 Liu, Wang, Yang and Pubu. 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:
Fuyuan Yang, School of Basic Medicine, Yangtze University Health Science Center, Jingzhou, Hubei, China., Jingzhou, Hubei, China., China
Ciren Pubu, Shannan Maternal and Child Health Hospital, Naidong District, Shannan, China, 山南市, China

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