Int J Biol Sci 2022; 18(14):5405-5414. doi:10.7150/ijbs.75876 This issue

Review

The Role of IL-6 in Fibrotic Diseases: Molecular and Cellular Mechanisms

Yanxia Li, Jing Zhao, Yuan Yin, Ke Li, Chenchen Zhang, Yajuan Zheng

Department of Ophthalmology, The Second Hospital of Jilin University, Jilin University, Changchun, China

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Citation:
Li Y, Zhao J, Yin Y, Li K, Zhang C, Zheng Y. The Role of IL-6 in Fibrotic Diseases: Molecular and Cellular Mechanisms. Int J Biol Sci 2022; 18(14):5405-5414. doi:10.7150/ijbs.75876. Available from https://www.ijbs.com/v18p5405.htm

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Abstract

Graphic abstract

Fibrosis is a detrimental outcome of most chronic inflammatory disorders and is defined by the buildup of excess extracellular matrix (ECM) components, which eventually leads to organ failure and death. Interleukin 6 (IL-6) is promptly produced by immune cells in response to tissue injuries and has a wide range of effects on cellular processes such as acute responses, hematopoiesis, and immune reactions. Furthermore, high levels of IL-6 have been found in a variety of chronic inflammatory disorders characterized by fibrosis, and this factor plays a significant role in fibrosis in various organs via Janus kinase/signal transducer and activator of transcription 3 (JAK/STAT3) activation. Here, we review what is known about the role of IL-6 in fibrosis and why targeting IL-6 for fibrotic disease treatment makes sense.

Keywords: Interleukin 6, JAK, STAT3, fibrosis