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• W1965224599 endingPage "599" @default.
• W1965224599 startingPage "556" @default.
• W1965224599 abstract "Reperfusion therapy is the indispensable treatment of acute myocardial infarction (AMI) and must be applied as soon as possible to attenuate the ischemic insult. However, reperfusion is responsible for additional myocardial damage likely involving opening of the mitochondrial permeability transition pore (mPTP). A great part of reperfusion injury occurs during the first minute of reperfusion. The prolonged opening of mPTP is considered one of the endpoints of the cascade to myocardial damage, causing loss of cardiomyocyte function and viability. Opening of mPTP and the consequent oxidative stress due to reactive oxygen and nitrogen species (ROS/RNS) are considered among the major mechanisms of mitochondrial and myocardial dysfunction. Kinases and mitochondrial components constitute an intricate network of signaling molecules and mitochondrial proteins, which interact in response to stressors. Cardioprotective pathways are activated by stimuli such as preconditioning and postconditioning (PostC), obtained with brief intermittent ischemia or with pharmacological agents, which drastically reduce the lethal ischemia/reperfusion injury. The protective pathways converging on mitochondria may preserve their function. Protection involves kinases, adenosine triphosphate-dependent potassium channels, ROS signaling, and the mPTP modulation. Some clinical studies using ischemic PostC during angioplasty support its protective effects, and an interesting alternative is pharmacological PostC. In fact, the mPTP desensitizer, cyclosporine A, has been shown to induce appreciable protections in AMI patients. Several factors and comorbidities that might interfere with cardioprotective signaling are considered. Hence, treatments adapted to the characteristics of the patient (i.e., phenotype oriented) might be feasible in the future. Antioxid. Redox Signal. 18, 556–599. I. Introduction A. Acute myocardial infarction and reperfusion injury B. Strategies to reduce injury II. Mitochondrial Network A. Important kinases of mitochondrial network involved in I/R injury and cardioprotection 1. GSK-3β in cell survival 2. PKC family in the I/R scenario and cardioprotection 3. The role of STAT-3 in cardioprotection by PreC and PostC 4. Pim-1 kinase in the I/R scenario and cardioprotection 5. Bcl-2 family: interaction with mitochondria 6. AMP-activated protein kinase, a metabolic regulator in health and disease B. Important components of mitochondria in the network involved in I/R and cardioprotection 1. Mitochondrial permeability transition pore 2. Putative mitochondrial ATP-sensitive potassium channels 3. Mitochondrial Cx43 4. Mitochondrial uncoupling proteins C. ROS/RNS: from mitochondria to activation of kinases of the network III. Role of Mitochondria in Acute I/R Injury A. mPTP opening in acute I/R 1. Consequences of prolonged mPTP opening B. Prevention of prolonged mPTP opening C. Transient opening of mPTP can be protective D. Chronic ischemia and mitochondria IV. Cardioprotective Strategies Targeting Mitochondria in Acute I/R Injury A. PreC and PostC B. Redox signaling and acidosis in early reperfusion 1. Detrimental effects of excessive ROS 2. Beneficial effects of redox signaling and acidosis V. Timing and Targets of ROS Signaling in Cardioprotection A. ROS/RNS signaling may be modulated by antioxidants B. Role of SNO in regulating mitochondrial function in I/R and cardioprotection VI. Preservation of Functional and Morphological Integrity of Mitochondria by PostC VII. Summary of PreC and PostC Pathways United at Reperfusion VIII. The Second Window of Protection IX. Autophagy and Mitophagy X. Comorbidities, I/R, and Cardioprotection A. Mitochondria and MS 1. Cardioprotection in MS B. Cardioprotection in Aging C. Cardioprotection in hypertension and hypertrophy XI. Transition to the Clinical Setting A. The possible reasons of variable outcomes with ischemic PostC B. Pharmacological PostC C. Features of a successful cardioprotective approach in early reperfusion XII. Executive Summary and Conclusions" @default.
• W1965224599 created "2016-06-24" @default.
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• W1965224599 creator A5035882795 @default.
• W1965224599 creator A5045025514 @default.
• W1965224599 date "2013-02-10" @default.
• W1965224599 modified "2023-10-16" @default.
• W1965224599 title "Mitochondrial Pathways, Permeability Transition Pore, and Redox Signaling in Cardioprotection: Therapeutic Implications" @default.
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