Ischemic postconditioning protects heart against hypoxia-reoxygenation injury via opening of mitochondrial Ca2+-activated K+ channels

Jin, Chunhong; Wu, Jinrong; Okada, Takao

doi:10.1016/j.yjmcc.2008.09.690

Cited by 1 publication

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“…On the other hand, iPostC promotes acidosis and gradual oxygenation, which are necessary to generate ROS signaling and interfere with mPTP formation and opening [22,33]. Notably, the opening of mitochondrial Ca 2+ -activated K + (mitoK Ca ) and mitoK ATP channels was also related to the protective effects of iPostC in rabbit and rat hearts [34,35]. iPostC preserves mitochondrial ultrastructure and cardioprotection has also been associated with decreased mitochondrial oxidative stress and increased buffering capacity to overcome Ca 2+ overload and cytochrome C release in rat hearts subjected to I/R [24,36].…”

Section: Protecting the Mitochondria: The Key Target In Myocardial Ischemic Conditioningmentioning

confidence: 99%

Mitochondrial Quality Control in Cardiac-Conditioning Strategies against Ischemia-Reperfusion Injury

García-Niño

Zazueta

Buelna‐Chontal

et al. 2021

Life

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Mitochondria are the central target of ischemic preconditioning and postconditioning cardioprotective strategies, which consist of either the application of brief intermittent ischemia/reperfusion (I/R) cycles or the administration of pharmacological agents. Such strategies reduce cardiac I/R injury by activating protective signaling pathways that prevent the exacerbated production of reactive oxygen/nitrogen species, inhibit opening of mitochondrial permeability transition pore and reduce apoptosis, maintaining normal mitochondrial function. Cardioprotection also involves the activation of mitochondrial quality control (MQC) processes, which replace defective mitochondria or eliminate mitochondrial debris, preserving the structure and function of the network of these organelles, and consequently ensuring homeostasis and survival of cardiomyocytes. Such processes include mitochondrial biogenesis, fission, fusion, mitophagy and mitochondrial-controlled cell death. This review updates recent advances in MQC mechanisms that are activated in the protection conferred by different cardiac conditioning interventions. Furthermore, the role of extracellular vesicles in mitochondrial protection and turnover of these organelles will be discussed. It is concluded that modulation of MQC mechanisms and recognition of mitochondrial targets could provide a potential and selective therapeutic approach for I/R-induced mitochondrial dysfunction.

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Section: Protecting the Mitochondria: The Key Target In Myocardial Ischemic Conditioningmentioning

confidence: 99%

Mitochondrial Quality Control in Cardiac-Conditioning Strategies against Ischemia-Reperfusion Injury

García-Niño

Zazueta

Buelna‐Chontal

et al. 2021

Life

View full text Add to dashboard Cite

show abstract

Ischemic postconditioning protects heart against hypoxia-reoxygenation injury via opening of mitochondrial Ca2+-activated K+ channels

Cited by 1 publication

References 0 publications

Mitochondrial Quality Control in Cardiac-Conditioning Strategies against Ischemia-Reperfusion Injury

Mitochondrial Quality Control in Cardiac-Conditioning Strategies against Ischemia-Reperfusion Injury

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