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

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 pathogenesis 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.