Ferroptosis turns 10: Emerging mechanisms, physiological functions, and therapeutic applications.
By Brent R. Stockwell. Cell, 2022
2,524 citations recorded by the source corpus.
Ferroptosis, a form of cell death driven by iron-dependent lipid peroxidation, was identified as a distinct phenomenon and named a decade ago. Ferroptosis has been implicated in a broad set of biological contexts, from development to aging, immunity, and cancer. This review describes key regulators of this form of cell death within a framework of metabolism, ROS biology, and iron biology. Key concepts and major unanswered questions in the ferroptosis field are highlighted. The next decade promises to yield further breakthroughs in the mechanisms governing ferroptosis and additional ways of harnessing ferroptosis for therapeutic benefit.
Subfields: Cancer Research, Molecular Biology, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/0763935a9ca5309860c9422ef5f00f60987ec0a1
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In Cancer Research
In Molecular Biology
In Pulmonary and Respiratory Medicine
- Brent R. Stockwell
- Deguang Liang
- Furong Zeng
- Yu Meng
- Yihuang Liu
- Guangtong Deng
- Xiang Chen
- Yuming Sun
Citations in the corpus
- The cell biology of ferroptosis (2024, neutral): “Selenium can enter the cell by endocytosis of the liver-secreted, selenium-containing carrier protein selenoprotein P, which is bound and endocytosed by cell surface receptors such as the LDL receptor-related protein 8 (LRP8) 63–65 .”
- Targeting p53 pathways: mechanisms, structures and advances in therapy (2023, background): “123 – 125 p53 was reported to inhibit cystine uptake and promote ferroptosis by transcriptional repression the expression of SLC7A11 which is a key component of the cystine-glutamate antiporter.”
- Ferroptosis in cancer: from molecular mechanisms to therapeutic strategies (2024, background): “12,13 On the other hand, cancer cells, in order to support their survival, can evolve several mechanisms to evade host ferroptosis, which provides vulnerable targets for ferroptosis-based therapy.”
- Ferroptosis surveillance independent of GPX4 and differentially regulated by sex hormones (2023, background): “Multiple surveillance mechanisms have evolved to suppress cellular PL peroxidation and subsequent ferroptosis, making these mechanisms pivotal points for ferroptosis regulation.(1,2) GPX4 and various RTA-generating enzymes mediate two well-characterized surveillance mechanisms.”