2023
DOI: 10.1007/s11684-023-0992-z
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Zooming in and out of ferroptosis in human disease

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Cited by 41 publications
(21 citation statements)
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“…Then, lipid radicals react with oxygen molecules to form a lipid peroxyl radical, which then reacts with nearby PUFAs to cause lipid peroxidation. This captures its hydrogen atoms and generates two new products called hydroperoxides and new lipid atomic groups, which lead to a chain reaction, generating many lipid peroxides, destroying the cell membrane, and causing ferroptosis [ 51 ]. 4-Hydroxynonenal (4-HNE) and malondialdehyde (MDA) are key biological biomarkers for verifying the occurrence of ferroptosis and lipid peroxidation.…”
Section: Mechanism Of Ferroptosismentioning
confidence: 99%
“…Then, lipid radicals react with oxygen molecules to form a lipid peroxyl radical, which then reacts with nearby PUFAs to cause lipid peroxidation. This captures its hydrogen atoms and generates two new products called hydroperoxides and new lipid atomic groups, which lead to a chain reaction, generating many lipid peroxides, destroying the cell membrane, and causing ferroptosis [ 51 ]. 4-Hydroxynonenal (4-HNE) and malondialdehyde (MDA) are key biological biomarkers for verifying the occurrence of ferroptosis and lipid peroxidation.…”
Section: Mechanism Of Ferroptosismentioning
confidence: 99%
“…With the rapid development of techniques and methods, a series of key regulatory genes and pathways related to ferroptosis have been identified. In general, the three basic characteristics of ferroptosis are the accumulation of Fe 2+ , PL peroxidation, and imbalance of antioxidant system [ 5 ]. Therefore, we summarize the regulatory network of ferroptosis around three factors: iron metabolism, lipid metabolism, and antioxidant system.…”
Section: The Mechanisms Of Ferroptosismentioning
confidence: 99%
“…This result may be associated with the HO-1 mediated-enhancement of glutathione peroxidase 4 (GPX4) activity [ 35 ]. There are four main destinations of Fe 2+ in LIP [ 5 , 7 ]: (1) Fe 2+ is exported to extracellular space through FPN; (2) Fe 2+ is used in the synthesis of iron-containing proteins; (3) Fe 2+ binds to ferritin through the iron chaperone poly (rC) -binding protein 1 (PCBP1); and (4) Fe 2+ enters mitochondria via SLC25A28/37 for heme, mitochondrial ferritin, and iron-sulfur (Fe-S) clusters synthesis. Two pathways mainly regulate the intracellular iron metabolism [ 32 ].…”
Section: The Mechanisms Of Ferroptosismentioning
confidence: 99%
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“…In about ten years of research investigations, ferroptosis emerged as a type of cell death with a pivotal role in preventing or even facilitating the progression of many diseases (reviewed in [ 1 , 2 , 3 ]). In particular, ferroptosis is now considered a good therapeutic option to treat multiple forms of cancer and arrest tumor growth [ 3 , 4 , 5 ], as well as a causal factor in neurodegenerative disorders [ 6 ], senescence/aging [ 7 ], different blood diseases [ 8 ], and kidney- and ischemia-reperfusion injuries [ 9 , 10 ].…”
Section: Introductionmentioning
confidence: 99%