Ferroptosis: molecular mechanisms and health implications

Daolin Tang, Xin Chen, Rui Kang, Guido Kroemer

Research output: Contribution to journalReview articlepeer-review

96 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)107-125
Number of pages19
JournalCell Research
Volume31
Issue number2
DOIs
StatePublished - Feb 2021

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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