ArticleNature communications2025
Attenuated growth factor signaling during cell death initiation sensitizes membranes towards peroxidation.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
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- Reorganization of Innate Immune Cell Lipid Profiles by Bioinspired Meroterpenoids to Limit Inflammation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
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- Hypoxia-mediated chromatin accessibility reprogramming of CA9 induces treatment resistance in colorectal mucinous adenocarcinoma.Journal of gastroenterology · 2026Article
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- NMR-Guided Discovery of Luvunga D: A Novel Propellane-Type Limonoid fromAntioxidants (Basel, Switzerland) · 2026Article
- Metabolic stress sensing by epithelial RXRα links westernization of diet with Crohn's disease.Cell metabolism · 2026Article
- NewInternational journal of molecular sciences · 2026Article
- Evaluation of soluble transferrin receptor and malondialdehyde levels associated with ferroptosis in children with familial Mediterranean fever in remission.Revista da Associacao Medica Brasileira (1992) · 2026Article
- Synthesis of Ethylphosphonate Curcumin Mimics: Substituents Allow Switching Between Cytotoxic and Cytoprotective Activities.Antioxidants (Basel, Switzerland) · 2025Article
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Authors and funding
35 authors.
Funding
Abstract
Cell death programs such as apoptosis and ferroptosis are associated with aberrant redox homeostasis linked to lipid metabolism and membrane function. Evidence for cross-talk between these programs is emerging. Here, we show that cytotoxic stress channels polyunsaturated fatty acids via lysophospholipid acyltransferase 12 into phospholipids that become susceptible to peroxidation under additional redox stress. This reprogramming is associated with altered acyl-CoA synthetase isoenzyme expression and caused by a decrease in growth factor receptor tyrosine kinase (RTK)-phosphatidylinositol-3-kinase signaling, resulting in suppressed fatty acid biosynthesis, for specific stressors via impaired Akt-SREBP1 activation. The reduced availability of de novo synthesized fatty acids favors the channeling of polyunsaturated fatty acids into phospholipids. Growth factor withdrawal by serum starvation mimics this phenotype, whereas RTK ligands counteract it. We conclude that attenuated RTK signaling during cell death initiation increases cells' susceptibility to oxidative membrane damage at the interface of apoptosis and alternative cell death programs.
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