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Abstract
Ferroptosis was recently identified as an iron-dependent regulatory necrosis process mediated by polyunsaturated fatty acid (PUFA) peroxidation. The pivotal events related to oxidative stress in ferroptosis include direct or indirect glutathione peroxidase 4 (GPX4) inhibition, ferrous iron overload, and lipid peroxidation. The links between ferroptosis and multiple pathological processes including tumor and cardiovascular system disease have become increasingly apparent, and the mechanisms and compounds involved in ferroptosis, such as reduction of coenzyme Q10 (ubiquinone/CoQ10), are gradually emerging. Current reports have revealed crossroads between ferroptosis and other multiple responses. This overview of the current research illuminates the mechanisms involving ferroptosis-related compounds and emphasizes the crosstalk between ferroptosis and other responses, including mitochondrial damage, endoplasmic reticulum stress (ER stress), autophagy, and the release of damage-associated molecular patterns (DAMPs), to reveal the intersections of regulatory mechanisms. This review also outlines the discovery, characterization, and pathological relevance of ferroptosis and notes controversial elements in ferroptosis-related mechanisms, such as nuclear factor E2-related factor 2 (Nrf2), sequestosome 1 (p62/SQSTM1), and heat shock protein family A member 5 (HSPA5). We hope our inferences will supply a partial reference for disorder prevention and treatment.
Highlights
Cell death is split into two mutually independent facets by the Nomenclature Committee on Cell Death (NCCD) in terms of a functional distinction: accidental cell death (ACD) and regulated cell death (RCD) [1]
Ferroptosis, a form of RCD that is the focus of increasing research attention, is a type of regulatory necrosis mediated by iron-dependent and polyunsaturated fatty acid (PUFA) peroxidation, which distinguishes it from other types of programmed cell death (PCD) in terms of morphology, biochemistry, and genetics [2]
These characteristics can be distinguished from the concentrated chromosomes occurring in apoptosis, the swollen cytoplasm and organelles and broken plasmalemma occurring in necrosis, and the doublemembrane vesicles occurring in autophagy [1, 2, 6]. (2) Biochemically, the specific aspects of ferroptosis include the accumulation of ferrous irons and reactive oxygen species (ROS) and the reduction of cysteine and glutathione (GSH)
Summary
Cell death is split into two mutually independent facets by the Nomenclature Committee on Cell Death (NCCD) in terms of a functional distinction: accidental cell death (ACD) and regulated cell death (RCD) [1]. RCD, in contrast, involves tremendous genetically encoded networks of molecular mechanisms and can be regulated by genetic or pharmacologic interference. RCD is termed programmed cell death (PCD) and includes apoptosis, necrosis, and autophagy, among other pathways [1]. Ferroptosis, a form of RCD that is the focus of increasing research attention, is a type of regulatory necrosis mediated by iron-dependent and polyunsaturated fatty acid (PUFA) peroxidation, which distinguishes it from other types of PCD in terms of morphology, biochemistry, and genetics [2]
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