Ferroptosis at the intersection of lipid metabolism and cellular signaling
By Deguang Liang, Alexander M. Minikes, Xuejun Jiang. Molecules and Cells, 2022
1,169 citations recorded by the source corpus.
SUMMARY Ferroptosis, a newly emerged form of regulated necrotic cell death, has been demonstrated to play an important role in multiple diseases including cancer, neurodegeneration, and ischemic organ injury. Mounting evidence also suggests its potential physiological function in tumor suppression and immunity. Execution of ferroptosis is driven by iron-dependent phospholipid peroxidation. As such, metabolism of biological lipids regulates ferroptosis via controlling phospholipid peroxidation, as well as various other cellular processes relevant to phospholipid peroxidation. In this review, we will provide a comprehensive analysis by focusing on how lipid metabolism impacts the initiation, propagation, and termination of phospholipid peroxidation, how multiple signal transduction pathways communicate with ferroptosis via modulating lipid metabolism, and how such intimate crosstalk of ferroptosis with lipid metabolism and related signaling pathways can be exploited for the development of rational therapeutic strategies.
Subfields: Cancer Research, Molecular Biology, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/690bfd3cdba68695c17e81f842c7600c47d0da7a
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Citations in the corpus
- The cell biology of ferroptosis (2024, neutral): “The execution of ferroptosis involves the peroxidation of PUFA-containing phospholipids and the formation of lipid hydroperoxides 14,15 .”
- Ferroptosis surveillance independent of GPX4 and differentially regulated by sex hormones (2023, background): “Because the composition of plasma membrane PL determines ferroptosis sensitivity, enzymatic components of Lands’ cycle are potential regulators of ferroptosis.(30) Indeed LPCAT3 (MBOAT5), another member of the MBOAT family, promotes ferroptosis by incorporating PUFAs into PLs to increase the level o”