The emerging roles of ferroptosis in organ fibrosis and its potential therapeutic effect

被引:20
作者
Huang, Xuege [1 ]
Song, Yahui [1 ]
Wei, Lin [1 ]
Guo, Jing [2 ]
Xu, Wei [1 ]
Li, Min [1 ]
机构
[1] Soochow Univ, Inst Biol & Med Sci, Bldg 703,199 Ren Ai Rd, Suzhou 215123, Peoples R China
[2] Stanford Univ, Sch Med, Dept Microbiol & Immunol, Stanford, CA 94305 USA
关键词
Ferroptosis; Iron; Lipid peroxidation; Organ fibrosis; CELL-DEATH; SIGNALING PATHWAY; LIVER FIBROSIS; MECHANISMS; PEROXIDATION; METABOLISM; ACTIVATION; INDUCTION; REGULATOR; DISEASE;
D O I
10.1016/j.intimp.2023.109812
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Fibrosis refers to the process of excessive deposition of extracellular matrix (ECM) proteins, eventually leading to excessive scar formation. Fibrotic diseases can occur in many organs and result in high mortality. Currently, there is no effective treatment for fibrosis. As a new form of regulatory cell death (RCD), ferroptosis is mainly mediated by iron overload and lipid peroxidation. Emerging evidence shows that ferroptosis is involved in the patho-genesis of fibrotic diseases. Generally, ferroptosis of parenchymal cells exacerbates the progression of fibrosis, while ferroptosis of myofibroblasts may ameliorate it. Therefore, studying the mechanisms of ferroptosis in fibrosis and targeting ferroptosis in certain cells can provide valuable insights into the pathogenesis of fibrotic diseases. In the present review, we summarized the mechanisms and regulators of ferroptosis and then described the mechanism of fibrosis and the role of ferroptosis in fibrotic diseases, including liver fibrosis, renal fibrosis, pulmonary fibrosis, and myocardial fibrosis.
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页数:9
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