Ferroptosis:molecular mechanisms and health implications

• 作 者: Daolin Tang Xin Chen Guido Kroemer Rui Kang
• 机 构: Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation
• 出 处: 细胞研究（英文版）
• 发表日期: 2021年2期

Cell death can be executed through different subroutines.Since the description of ferroptosis as an iron-dependent form of non-apoptotic cell death in 2012,there has been mounting interest in the process and function of ferroptosis.Ferroptosis can occur through two major pathways,the extrinsic or transporter-dependent pathway and the intrinsic or enzyme-regulated pathway.Ferroptosis is caused by a redox imbalance between the production of oxidants and antioxidants,which is driven by the abnormal expression and activity of multiple redox-active enzymes that produce or detoxify free radicals and lipid oxidation products.Accordingly,ferroptosis is precisely regulated at multiple levels,including epigenetic,transcriptional,posttranscriptional and posttranslational layers.The transcription factor NFE2L2 plays a central role in upregulating anti-ferroptotic defense,whereas selective autophagy may promote ferroptotic death.Here,we review current knowledge on the integrated molecular machinery of ferroptosis and describe how dysregulated ferroptosis is involved in cancer,neurodegeneration,tissue injury,inflammation,and infection.