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Journal ArticleDOI

Ferroptosis and its emerging roles in cardiovascular diseases.

TLDR
Ferroptosis is a new form of regulated cell death (RCD) driven by iron-dependent lipid peroxidation, which is morphologically and mechanistically distinct from other forms of RCD including apoptosis, autophagic cell death, pyroptotic and necroptosis as mentioned in this paper.
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This article is published in Pharmacological Research.The article was published on 2021-02-03. It has received 80 citations till now. The article focuses on the topics: Necroptosis.

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Verification of ferroptosis and pyroptosis and identification of PTGS2 as the hub gene in human coronary artery atherosclerosis.

TL;DR: In this article, the authors investigated the expression of ferroptosis-related proteins in human coronary arteries and analyzed correlation with severity of atherosclerosis and clarified the interactions between proteins and possible mechanisms of atherosis.
Journal ArticleDOI

Targeting Ferroptosis against Ischemia/Reperfusion Cardiac Injury.

TL;DR: In this paper, the role of ferroptosis inhibition to prevent heart IRI was analyzed in patients with acute myocardial infarction, with special reference to Lip-1 as a promising drug in this clinicopathological context.
Journal ArticleDOI

Insight into Crosstalk between Ferroptosis and Necroptosis: Novel Therapeutics in Ischemic Stroke

Abstract: Ferroptosis is a nonapoptotic form of cell death characterized by iron-dependent accumulation of lipid hydroperoxides to lethal levels. Necroptosis, an alternative form of programmed necrosis, is regulated by receptor-interacting protein (RIP) 1 activation and by RIP3 and mixed-lineage kinase domain-like (MLKL) phosphorylation. Ferroptosis and necroptosis both play important roles in the pathological progress in ischemic stroke, which is a complex brain disease regulated by several cell death pathways. In the past few years, increasing evidence has suggested that the crosstalk occurs between necroptosis and ferroptosis in ischemic stroke. However, the potential links between ferroptosis and necroptosis in ischemic stroke have not been elucidated yet. Hence, in this review, we overview and analyze the mechanism underlying the crosstalk between necroptosis and ferroptosis in ischemic stroke. And we find that iron overload, one mechanism of ferroptosis, leads to mitochondrial permeability transition pore (MPTP) opening, which aggravates RIP1 phosphorylation and contributes to necroptosis. In addition, heat shock protein 90 (HSP90) induces necroptosis and ferroptosis by promoting RIP1 phosphorylation and suppressing glutathione peroxidase 4 (GPX4) activation. In this work, we try to deliver a new perspective in the exploration of novel therapeutic targets for the treatment of ischemic stroke.
Journal ArticleDOI

Epigallocatechin-3-gallate pretreatment alleviates doxorubicin-induced ferroptosis and cardiotoxicity by upregulating AMPKα2 and activating adaptive autophagy.

TL;DR: In this paper, epigallocatechin-3-gallate pretreatment could effectively decrease iron accumulation, inhibit oxidative stress and abnormal lipid metabolism, and thereby alleviate Dox cardiotoxicity-induced ferroptosis and protect the myocardium.
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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AMPK: a nutrient and energy sensor that maintains energy homeostasis

TL;DR: AMP-activated protein kinase conserves ATP levels through the regulation of processes other than metabolism, such as the cell cycle and neuronal membrane excitability.
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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.
Journal ArticleDOI

Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.

Lorenzo Galluzzi, +186 more
TL;DR: The Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives.
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