Affiliation:
1. Department of Translational Biomedicine and Neuroscience (DiBraiN), Section of Human Anatomy and Histology, University of Bari “Aldo Moro”, 70124 Bari, Italy
Abstract
Fibrosis is the end result of persistent inflammatory responses induced by a variety of stimuli, including chronic infections, autoimmune reactions, and tissue injury. Fibrotic diseases affect all vital organs and are characterized by a high rate of morbidity and mortality in the developed world. Until recently, there were no approved antifibrotic therapies. In recent years, high levels of interleukin-17 (IL-17) have been associated with chronic inflammatory diseases with fibrotic complications that culminate in organ failure. In this review, we provide an update on the role of IL-17 in fibrotic diseases, with particular attention to the most recent lines of research in the therapeutic field represented by the epigenetic mechanisms that control IL-17 levels in fibrosis. A better knowledge of the IL-17 signaling pathway implications in fibrosis could design new strategies for therapeutic benefits.
Reference131 articles.
1. Shared and distinct mechanisms of fibrosis;Distler;Nat. Rev. Rheumatol.,2019
2. Scraping fibrosis: Expressway to the core of fibrosis;Mehal;Nat. Med.,2011
3. The immunology of fibrosis;Wick;Annu. Rev. Immunol.,2013
4. Fibrosis: From mechanisms to medicines;Enderson;Nature,2020
5. Miao, H., Wu, X.Q., Zhang, D.D., Wang, Y.N., Guo, Y., Li, P., Xiong, Q., and Zhao, Y.Y. (2021). Deciphering the cellular mechanisms underlying fibrosis-associated diseases and therapeutic avenues. Pharmacol. Res., 163.
Cited by
2 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献