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The pathogenesis of organ fibrosis: Focus on necroptosis
Author(s) -
Hao Min,
Han Xin,
Yao Zhouhui,
Zhang Han,
Zhao Mengting,
Peng Mengyun,
Wang Kuilong,
Shan Qiyuan,
Sang Xianan,
Wu Xin,
Wang Lu,
Lv Qiang,
Yang Qiao,
Bao Yini,
Kuang Haodan,
Zhang Hongyan,
Cao Gang
Publication year - 2023
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/bph.15952
Subject(s) - necroptosis , fibrosis , hepatic stellate cell , programmed cell death , autophagy , myofibroblast , biology , extracellular matrix , cancer research , cell type , apoptosis , medicine , pathology , microbiology and biotechnology , cell , biochemistry , genetics
Fibrosis is a common process of tissue repair response to multiple injuries in all chronic progressive diseases, which features with excessive deposition of extracellular matrix. Fibrosis can occur in all organs and tends to be nonreversible with the progress of the disease. Different cells types in different organs are involved in the occurrence and development of fibrosis, that is, hepatic stellate cells, pancreatic stellate cells, fibroblasts and myofibroblasts. Various types of programmed cell death, including apoptosis, autophagy, ferroptosis and necroptosis, are closely related to organ fibrosis. Among these programmed cell death types, necroptosis, an emerging regulated cell death type, is regarded as a huge potential target to ameliorate organ fibrosis. In this review, we summarize the role of necroptosis signalling in organ fibrosis and collate the small molecule compounds targeting necroptosis. In addition, we discuss the potential challenges, opportunities and open questions in using necroptosis signalling as a potential target for antifibrotic therapies. LINKED ARTICLES This article is part of a themed issue on Translational Advances in Fibrosis as a Therapeutic Target. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v180.22/issuetoc