Regulation of ferroptosis by lipid metabolism

Lauren E Pope; Scott J Dixon

doi:10.1016/j.tcb.2023.05.003

Regulation of ferroptosis by lipid metabolism

Trends Cell Biol. 2023 Dec;33(12):1077-1087. doi: 10.1016/j.tcb.2023.05.003. Epub 2023 Jul 3.

Authors

Lauren E Pope¹, Scott J Dixon²

Affiliations

¹ Department of Biology, Stanford University, Stanford, CA, USA.
² Department of Biology, Stanford University, Stanford, CA, USA. Electronic address: sjdixon@stanford.edu.

PMID: 37407304
PMCID: PMC10733748 (available on 2024-12-01)
DOI: 10.1016/j.tcb.2023.05.003

Abstract

Ferroptosis is an iron-dependent lethal mechanism that can be activated in disease and is a proposed target for cancer therapy. Ferroptosis is defined by the overwhelming accumulation of membrane lipid peroxides. Ferroptotic lipid peroxidation is initiated on internal membranes and then appears at the plasma membrane, triggering lethal ion imbalances and membrane permeabilization. Sensitivity to ferroptosis is governed by the levels of peroxidizable polyunsaturated lipids and associated lipid metabolic enzymes. A different network of enzymes and endogenous metabolites restrains lipid peroxidation by interfering with the initiation or propagation of this process. This emerging understanding is informing new approaches to treat disease by modulating lipid metabolism to enhance or inhibit ferroptosis.

Keywords: MUFA; PUFA; cell death; ferroptosis; lipid; metabolism.

Publication types

Review
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, N.I.H., Extramural

MeSH terms

Cell Death
Ferroptosis*
Humans
Lipid Metabolism
Lipid Peroxidation
Lipid Peroxides

Substances

Lipid Peroxides

Abstract

Publication types

MeSH terms

Substances

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