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Open AccessJournal ArticleDOI

Dietary Lipids Induce Ferroptosis in Caenorhabditiselegans and Human Cancer Cells.

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TLDR
It is shown that dietary ingestion of the polyunsaturated fatty acid (PUFA) dihomogamma-linolenic acid (DGLA) can trigger germ-cell ferroptosis and sterility in the nematode Caenorhabditis elegans and indicates that endogenous ether lipids act to prevent this nonapoptotic cell fate.
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This article is published in Developmental Cell.The article was published on 2020-07-10 and is currently open access. It has received 118 citations till now.

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Journal ArticleDOI

The Metabolic Underpinnings of Ferroptosis.

TL;DR: There has been overwhelming interest in the last few years aiming for a better molecular understanding of the ferroptotic death process, which emerges to be the root cause of a number of diseases.
Journal ArticleDOI

Ferroptosis turns 10: Emerging mechanisms, physiological functions, and therapeutic applications

Brent R. Stockwell
- 01 Jul 2022 - 
TL;DR: Ferroptosis, a form of cell death driven by iron-dependent lipid peroxidation, was identified as a distinct phenomenon and named a decade ago as discussed by the authors , which has been implicated in a broad set of biological contexts, from development to aging, immunity, and cancer.
Journal ArticleDOI

Clinical and Biological Significances of a Ferroptosis-Related Gene Signature in Glioma.

TL;DR: Results show that the gene risk signature associated with clinical features can be as an independent prognostic indicator in glioma patients and can potentially predict the outcome of gliomas patients.
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Kaempferol Ameliorates Oxygen-Glucose Deprivation/Reoxygenation-Induced Neuronal Ferroptosis by Activating Nrf2/SLC7A11/GPX4 Axis

TL;DR: Results suggest that ferroptosis may be a significant cause of cell death associated with oxygen-glucose deprivation/reperfusion-induced neuronal injury and the effects of kaempferol on ferroPTosis in OGD/R-treated neurons.
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Emerging Roles of Energy Metabolism in Ferroptosis Regulation of Tumor Cells.

TL;DR: In this article, the regulatory impact of tumor specific metabolic aberrations is systematically characterized, such as rewired glucose metabolism and metabolic compensation through glutamine utilization on ferroptosis and analyzed the underlying molecular mechanisms.
References
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Journal ArticleDOI

Ferroptosis: An Iron-Dependent Form of Nonapoptotic Cell Death

TL;DR: This paper identified the small molecule ferrostatin-1 as a potent inhibitor of ferroptosis in cancer cells and glutamate-induced cell death in organotypic rat brain slices, suggesting similarities between these two processes.
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Regulation of Ferroptotic Cancer Cell Death by GPX4

TL;DR: Targeted metabolomic profiling and chemoproteomics revealed that GPX4 is an essential regulator of ferroptotic cancer cell death and sensitivity profiling in 177 cancer cell lines revealed that diffuse large B cell lymphomas and renal cell carcinomas are particularly susceptible to GPx4-regulated ferroPTosis.
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ACSL4 dictates ferroptosis sensitivity by shaping cellular lipid composition

TL;DR: Pharmacological targeting of ACSL4 with thiazolidinediones, a class of antidiabetic compound, ameliorated tissue demise in a mouse model of ferroptosis, suggesting that ACSL 4 inhibition is a viable therapeutic approach to preventing ferroPTosis-related diseases.
Journal ArticleDOI

Ferroptosis: Death by Lipid Peroxidation

TL;DR: The discovery of ferroptosis, the mechanism of ferraptosis regulation, and its increasingly appreciated relevance to both normal and pathological physiology are summarized.
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