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Cited by 787

The DOI matches its Crossref record; 130 of the 130 references it cites were found in a registry or an index.

Signaling pathways and defense mechanisms of ferroptosis

Open access
Liu, Jiao, Kang, Rui, Tang, Daolin·2022·The FEBS Journal

Abstract

As a type of lytic cell death driven by unrestricted lipid peroxidation and subsequent plasma membrane damage, ferroptosis occurs and develops because of sophisticated signals and regulatory mechanisms. The reactive oxygen species (ROS) used to initiate ferroptosis come from a variety of sources, including iron‐mediated Fenton reactions, mitochondrial ROS, and membrane‐associated ROS driven by the NOX protein family. Polyunsaturated fatty acid‐containing phospholipids are the main substrates of lipid peroxidation in ferroptosis, which is positively regulated by enzymes, such as ACSL4, LPCAT3, ALOXs, or POR. Selective activation of autophagic degradation pathways promotes ferroptosis by increasing iron accumulation to cause lipid peroxidation. In contrast, system xc–‐glutathione–GPX4 axis plays a central role in limiting lipid peroxidation, although other antioxidants (such as coenzyme Q10 and tetrahydrobiopterin) can also inhibit ferroptosis. A main nuclear mechanism of cell defense against ferroptosis is the activation of the NFE2L2‐dependent antioxidant response by transcriptionally upregulating the expression of antioxidants or cytoprotective genes. Additionally, the membrane damage caused by ferroptotic stimulus can be repaired by ESCRT‐III‐dependent membrane scission machinery. In this review, we summarize recent progress in understanding the signaling pathways and defense mechanisms of ferroptosis.

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Metadata

Authors
Liu, J., Kang, R., & Tang, D.
Venue
The FEBS Journal
Publisher
Wiley
Published
2021-06-17
Volume
289
Issue
22
Pages
7038-7050
ISSN
  • 1742-464X (ISSN-L)
  • 1742-4658
OpenAlex
W3169941200
Cited by
787
References
130
FWCI
51.77
Type
journal article
Language
en
Open access
bronze

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