
DOI . ORG {
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Title[redir]:
Targeting ferroptosis opens new avenues for the development of novel therapeutics | Signal Transduction and Targeted Therapy
Description:
Ferroptosis is an iron-dependent form of regulated cell death with distinct characteristics, including altered iron homeostasis, reduced defense against oxidative stress, and abnormal lipid peroxidation. Recent studies have provided compelling evidence supporting the notion that ferroptosis plays a key pathogenic role in many diseases such as various cancer types, neurodegenerative disease, diseases involving tissue and/or organ injury, and inflammatory and infectious diseases. Although the precise regulatory networks that underlie ferroptosis are largely unknown, particularly with respect to the initiation and progression of various diseases, ferroptosis is recognized as a bona fide target for the further development of treatment and prevention strategies. Over the past decade, considerable progress has been made in developing pharmacological agonists and antagonists for the treatment of these ferroptosis-related conditions. Here, we provide a detailed overview of our current knowledge regarding ferroptosis, its pathological roles, and its regulation during disease progression. Focusing on the use of chemical tools that target ferroptosis in preclinical studies, we also summarize recent advances in targeting ferroptosis across the growing spectrum of ferroptosis-associated pathogenic conditions. Finally, we discuss new challenges and opportunities for targeting ferroptosis as a potential strategy for treating ferroptosis-related diseases.
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Keywords {🔍}
pubmed, ferroptosis, google, scholar, cas, cancer, cell, central, cells, iron, shown, gpx, death, lipid, disease, pathway, diseases, chem, injury, target, targeting, role, biol, protein, inhibitors, inhibitor, peroxidation, tumor, inhibiting, addition, metabolism, activity, recently, res, clinical, including, drug, mice, studies, damage, glutathione, sci, therapy, gsh, med, nature, treating, cellular, nanoparticles, wang,
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cso-ss-cy7-hex/spion/srfn319 crispr/cas9-based gene editing nature portfolio privacy policy advertising akt/gsk-3beta/nrf2 pathway l-g-glutamyl-p-nitroanilide therapeutic index monocyte/macrophage-specific scavenger receptor hmg-coa 3-hydroxy-3-methylglutaryl-coa p62-keap1-nrf2 signaling pathway apoptosis-inducing factor-homologous mitochondrion ferroptosis-focused translational research social media p62-keap1-nrf2 signalling pathway gene editing oncogenic-ras-harboring cancer cells tfr1-specific antibody 3f3-fma fenton-reaction-acceleratable magnetic nanoparticles activating sirt3-sod2/gpx4 pathway hmgcr 3-hydroxy-3-methylglutaryl-coa reductase febs open bio p62-keap1-nrf2 pathway protects ischemia-induced myocardial injury260 reprints /r-induced cerebral injury259 sirt1/nrf2/ho-1/gpx4 pathway ischemia-induced myocardial damage oxalate crystal‒induced models gpx4-knockout fsp1-overexpressing cells hepatic ischemia-reperfusion injury hepatic ischemia/reperfusion injury system xc–-gsh-gpx4 pathway oxalate crystal‒induced inflammation long-chain polyunsaturated bonds chemical tools imaging-guided photodynamic therapy triple-negative breast cancer small-molecule screening identifies opioid-induced delayed cardioprotection oxidant-enriched tumorigenic endothelial lf receptor‒mediated transcytosis 78 methionine/choline-deficient‒induced enzyme cystathionine beta-synthase cell line data encapsulated metal-organic network sudden-onset kidney failure 1-[ethan-1’ol]-2-methyl-3-hydroxypyridin-4 cbs cystathionine beta-synthase /r-induced acute damage
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headline:Targeting ferroptosis opens new avenues for the development of novel therapeutics
description:Ferroptosis is an iron-dependent form of regulated cell death with distinct characteristics, including altered iron homeostasis, reduced defense against oxidative stress, and abnormal lipid peroxidation. Recent studies have provided compelling evidence supporting the notion that ferroptosis plays a key pathogenic role in many diseases such as various cancer types, neurodegenerative disease, diseases involving tissue and/or organ injury, and inflammatory and infectious diseases. Although the precise regulatory networks that underlie ferroptosis are largely unknown, particularly with respect to the initiation and progression of various diseases, ferroptosis is recognized as a bona fide target for the further development of treatment and prevention strategies. Over the past decade, considerable progress has been made in developing pharmacological agonists and antagonists for the treatment of these ferroptosis-related conditions. Here, we provide a detailed overview of our current knowledge regarding ferroptosis, its pathological roles, and its regulation during disease progression. Focusing on the use of chemical tools that target ferroptosis in preclinical studies, we also summarize recent advances in targeting ferroptosis across the growing spectrum of ferroptosis-associated pathogenic conditions. Finally, we discuss new challenges and opportunities for targeting ferroptosis as a potential strategy for treating ferroptosis-related diseases.
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description:Ferroptosis is an iron-dependent form of regulated cell death with distinct characteristics, including altered iron homeostasis, reduced defense against oxidative stress, and abnormal lipid peroxidation. Recent studies have provided compelling evidence supporting the notion that ferroptosis plays a key pathogenic role in many diseases such as various cancer types, neurodegenerative disease, diseases involving tissue and/or organ injury, and inflammatory and infectious diseases. Although the precise regulatory networks that underlie ferroptosis are largely unknown, particularly with respect to the initiation and progression of various diseases, ferroptosis is recognized as a bona fide target for the further development of treatment and prevention strategies. Over the past decade, considerable progress has been made in developing pharmacological agonists and antagonists for the treatment of these ferroptosis-related conditions. Here, we provide a detailed overview of our current knowledge regarding ferroptosis, its pathological roles, and its regulation during disease progression. Focusing on the use of chemical tools that target ferroptosis in preclinical studies, we also summarize recent advances in targeting ferroptosis across the growing spectrum of ferroptosis-associated pathogenic conditions. Finally, we discuss new challenges and opportunities for targeting ferroptosis as a potential strategy for treating ferroptosis-related diseases.
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