
DOI . ORG {
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Title[redir]:
Insight into Crosstalk Between Mitophagy and Apoptosis/Necroptosis: Mechanisms and Clinical Applications in Ischemic Stroke | Current Medical Science
Description:
Ischemic stroke is a serious cerebrovascular disease with high morbidity and mortality. As a result of ischemia-reperfusion, a cascade of pathophysiological responses is triggered by the imbalance in metabolic supply and demand, resulting in cell loss. These cellular injuries follow various molecular mechanisms solely or in combination with this disorder. Mitochondria play a driving role in the pathophysiological processes of ischemic stroke. Once ischemic stroke occurs, damaged cells would respond to such stress through mitophagy. Mitophagy is known as a conservatively selective autophagy, contributing to the removal of excessive protein aggregates and damaged intracellular components, as well as aging mitochondria. Moderate mitophagy may exert neuroprotection against stroke. Several pathways associated with the mitochondrial network collectively contribute to recovering the homeostasis of the neurovascular unit. However, excessive mitophagy would also promote ischemia-reperfusion injury. Therefore, mitophagy is a double-edged sword, which suggests that maximizing the benefits of mitophagy is one of the direction of future efforts. This review emphasized the role of mitophagy in ischemic stroke, and highlighted the crosstalk between mitophagy and apoptosis/necroptosis.
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Keywords {π}
article, google, scholar, cas, mitophagy, mitochondrial, stroke, ischemic, cell, injury, med, biol, res, mitochondria, zhang, autophagy, ischemiareperfusion, mol, sci, parkin, cerebral, apoptosis, necroptosis, mechanisms, chen, wang, pink, yang, role, acute, death, front, medical, kun, xiong, disease, molecular, stress, therapeutic, target, brain, int, neural, regen, nat, activation, zhu, china, function, research,
Topics {βοΈ}
cerebral ischemia-reperfusion injury promote ischemia-reperfusion injury myocardial ischemia/reperfusion injury calcium-induced mitochondrial swelling drp1-activated mitochondrial fission pink1/parkin-mediated mitophagy clearance bnip3l/nix-mediated mitophagy protects glucocorticoid-induced synapse defects drp1/mff signaling pathway fluoride-induced abnormal fission steroid-induced osteocytes apoptosis maintaining er-mitochondrial contacts hypoxia-inducible factor induction risk factor-based approach fundc1-dependent mitophagy induced damage-induced mitochondrial localization current medical science article download pdf ischemia/reperfusion injury ischemia-reperfusion injury tissue-type plasminogen activator pro-apoptotic mitochondrial proteins site-specific interaction mapping activating bnip3-mediated mitophagy cerebral ischemia-reperfusion hypoxia-induced autophagy conventional kinase activity pink1/parkin-mediated mitophagy author kun xiong basic medical science xi-min hu hypoxic ischemic injury dynamin-related protein 1 inhibiting neuronal apoptosis cardiac ir injury acute ischemic stroke zi-xin li privacy choices/manage cookies ischemic stroke research excessive protein aggregates cerebral ischemic stroke ischemic brain damage early management strategies tissue plasminogen activator hainan medical university post-ischemic heart pink1/parkin pathway tpa protects neurons delayed neuronal death hypoxic/ischemic stress
Questions {β}
- Do pyroptosis, apoptosis, and necroptosis (PANoptosis) exist in cerebral ischemia?
- To mdivi-1 or not to mdivi-1: Is that the question?
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headline:Insight into Crosstalk Between Mitophagy and Apoptosis/Necroptosis: Mechanisms and Clinical Applications in Ischemic Stroke
description:Ischemic stroke is a serious cerebrovascular disease with high morbidity and mortality. As a result of ischemia-reperfusion, a cascade of pathophysiological responses is triggered by the imbalance in metabolic supply and demand, resulting in cell loss. These cellular injuries follow various molecular mechanisms solely or in combination with this disorder. Mitochondria play a driving role in the pathophysiological processes of ischemic stroke. Once ischemic stroke occurs, damaged cells would respond to such stress through mitophagy. Mitophagy is known as a conservatively selective autophagy, contributing to the removal of excessive protein aggregates and damaged intracellular components, as well as aging mitochondria. Moderate mitophagy may exert neuroprotection against stroke. Several pathways associated with the mitochondrial network collectively contribute to recovering the homeostasis of the neurovascular unit. However, excessive mitophagy would also promote ischemia-reperfusion injury. Therefore, mitophagy is a double-edged sword, which suggests that maximizing the benefits of mitophagy is one of the direction of future efforts. This review emphasized the role of mitophagy in ischemic stroke, and highlighted the crosstalk between mitophagy and apoptosis/necroptosis.
datePublished:2022-04-07T00:00:00Z
dateModified:2022-04-07T00:00:00Z
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headline:Insight into Crosstalk Between Mitophagy and Apoptosis/Necroptosis: Mechanisms and Clinical Applications in Ischemic Stroke
description:Ischemic stroke is a serious cerebrovascular disease with high morbidity and mortality. As a result of ischemia-reperfusion, a cascade of pathophysiological responses is triggered by the imbalance in metabolic supply and demand, resulting in cell loss. These cellular injuries follow various molecular mechanisms solely or in combination with this disorder. Mitochondria play a driving role in the pathophysiological processes of ischemic stroke. Once ischemic stroke occurs, damaged cells would respond to such stress through mitophagy. Mitophagy is known as a conservatively selective autophagy, contributing to the removal of excessive protein aggregates and damaged intracellular components, as well as aging mitochondria. Moderate mitophagy may exert neuroprotection against stroke. Several pathways associated with the mitochondrial network collectively contribute to recovering the homeostasis of the neurovascular unit. However, excessive mitophagy would also promote ischemia-reperfusion injury. Therefore, mitophagy is a double-edged sword, which suggests that maximizing the benefits of mitophagy is one of the direction of future efforts. This review emphasized the role of mitophagy in ischemic stroke, and highlighted the crosstalk between mitophagy and apoptosis/necroptosis.
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