Mitochondrial Metabolic Inhibition and Cardioprotection

Mitochondrial Metabolic Inhibition and Cardioprotection

Reperfusion is needed to initiate reflow of blood in cardiac arrest triggered by surgical intervention or pathologically-induced cardiac ischemia. However, subsequent reperfusion may lead not only to the recovery of ischemic cardiac tissue, but also to the paradoxical phenomenon of myocardial ischemia/reperfusion (IR) injury, including protracted organ recovery, myocardial stunning, and acute m...

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Mitochondrial metabolism revisited: a route to cardioprotection.

Ischaemic preconditioning confers strong protection against myocardial ischaemia–reperfusion injury. Although its therapeutic application in the case of acute coronary syndromes is not possible in general, the cellular and molecular processes leading to preconditioning protection may be of interest for the designing of cardioprotective therapies. Many cellular processes have been shown to be in...

Acetaminophen-mediated cardioprotection via inhibition of the mitochondrial permeability transition pore-induced apoptotic pathway.

Our laboratory has previously reported that acetaminophen confers functional cardioprotection following cardiac insult, including ischemia/reperfusion, hypoxia/reoxygenation, and exogenous peroxynitrite administration. In the present study, we further examined the mechanism of acetaminophen-mediated cardioprotection following ischemia/reperfusion injury. Langendorff-perfused guinea pig hearts w...

Inhibition of mitochondrial permeability transition pore restores the cardioprotection by postconditioning in diabetic hearts

BACKGROUND Cardiovascular risk factors, including diabetes mellitus may attenuate the cardioprotection by postconditioning. This study aimed to investigate the cardioprotective effect of ischemic-postconditioning (IPostC) against ischemia/reperfusion injury in normal and chronically type-1 diabetic rats and the effect of mitochondrial permeability transition pore (mPTP) inhibition in this field...