Abstract
Ferroptosis is a type of programmed cell death characterized by iron overload, oxidative stress, imbalance in lipid repair, and mitochondria-specific pathological manifestations. Growing number of molecular mechanisms and signaling pathways have been found to be involved in ferroptosis progression, including iron metabolism, amino acid metabolism, lipid metabolism, and energy metabolism. It is worth noting that ferroptosis is involved in the progression of fibrotic diseases such as liver cirrhosis, cardiomyopathy, and idiopathic pulmonary fibrosis, and inhibition of ferroptosis has acquired beneficial outcomes in rodent models, while studies on ferroptosis and renal fibrosis remains limited. Recent studies have revealed that targeting ferroptosis can effectively mitigate chronic kidney injury and renal fibrosis. Moreover, myofibroblasts suffer from ferroptosis during fiber and extracellular matrix deposition in the fibrotic cascade reaction and pharmacological modulation of ferroptosis shows great therapeutic effect on renal fibrosis. Here, we summarize the latest molecular mechanisms of ferroptosis from high-quality studies and review its therapeutic potential in renal fibrosis.