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- W182033340 abstract "The mitochondrion has evolved as an important organelle in determining cell survival and cell death. It is involved in a plethora of processes in mammalian cells including ATP production, steroid synthesis, and cell division and cell death. Indeed, mitochondrial dysfunction is associated with numerous human maladies including heart disease. Mitochondrial diseases have traditionally been attributed to defects in the electron transport chain (ETC), the major source of mitochondrial reactive oxygen species (ROS), a byproduct of mitochondrial respiration. Mitochondrial cation channels and exchangers function to maintain matrix homeostasis and are likely involved in modulating mitochondrial function in part by regulating O 2 •- generation. Insofar as mitochondria are involved in oxidative damage that leads to apoptosis, antioxidants and other therapeutic strategies that target the organelle appear to be a novel approach to alleviate some cardiovascular diseases. This novel approach has gained unprecedented attention recently with a significant potential for future therapeutic purpose. Whether mitochondria are targets or end effectors of cardiac pre- and post-conditioning remain unresolved. This brief review will provide the latest information gleaned from the literature on the role of mitochondria in pre- and post-conditioning during cardiac ischemia and reperfusion." @default.
- W182033340 created "2016-06-24" @default.
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- W182033340 date "2011-05-27" @default.
- W182033340 modified "2023-09-22" @default.
- W182033340 title "CARDIOPROTECTION BY PRE- AND POST-CONDITIONING: IMPLICATIONS FOR THE ROLE OF MITOCHONDRIA" @default.
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