Autophagy-Dependent Ferroptosis: Machinery and Regulation

Jiao Liu, Feimei Kuang, Guido Kroemer, Daniel J. Klionsky, Rui Kang, Daolin Tang

Research output: Contribution to journalReview articlepeer-review

58 Scopus citations

Abstract

Macroautophagy (hereafter referred to as autophagy) is an evolutionarily conserved cellular process capable of degrading various biological molecules (e.g., protein, glycogen, lipids, DNA, and RNA) and organelles (e.g., mitochondria, endoplasmic reticulum [ER] ribosomes, lysosomes, and micronuclei) via the lysosomal pathway. Ferroptosis is a type of oxidative stress-dependent regulated cell death associated with iron accumulation and lipid peroxidation. The recently discovered role of autophagy, especially selective types of autophagy (e.g., ferritinophagy, lipophagy, clockophagy, and chaperone-mediated autophagy), in driving cells toward ferroptotic death motivated us to explore the functional interactions between metabolism, immunity, and cell death. Here, we describe types of selective autophagy and discuss the regulatory mechanisms and signaling pathways of autophagy-dependent ferroptosis. We also summarize chemical modulators that are currently available for triggering or blocking autophagy-dependent ferroptosis and that may be developed for therapeutic interventions in human diseases.

Original languageEnglish (US)
Pages (from-to)420-435
Number of pages16
JournalCell Chemical Biology
Volume27
Issue number4
DOIs
StatePublished - Apr 16 2020

Keywords

  • autophagy
  • ferroptosis
  • network
  • regulated cell death
  • selective autophagy

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Medicine
  • Molecular Biology
  • Pharmacology
  • Drug Discovery
  • Clinical Biochemistry

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