Postconditioning has recently been described as a powerful cardioprotection that prevents
lethal reperfusion injury. Growing evidence suggests that mitochondrial permeability …

Postconditioning (PostC) may limit mitochondrial damage and apoptotic signaling. We
studied markers of apoptosis and mitochondrial protection in isolated rat hearts, which …

We hypothesized that low-pressure reperfusion may limit myocardial necrosis and attenuate
postischemic contractile dysfunction by inhibiting mitochondrial permeability transition pore …

Mitochondria have long been known to be the gatekeepers of cell fate. This is particularly so
in the response to acute ischaemia‐reperfusion injury (IRI). Following an acute episode of …

Both mitochondria and the sarcoplasmic reticulum (SR) are essential for myocardial
homeostasis and control of cardiac function. Uptake of Ca2+ from the cytosol into SR is …

Reperfusion may induce additional cell death in patients with acute myocardial infarction
receiving primary angioplasty or thrombolysis. Altered intracellular Ca2+ handling was …

Several signal transduction pathways are activated by cardioprotective stimuli, including
ischemic or pharmacological postconditioning. These pathways converge on a common …

In ischemia–reperfusion injuries, elevated calcium and reactive oxygen species (ROS)
induce mitochondrial permeability transition (mPT), which plays a pivotal role in mediating …

The concept of reperfusion injury has been a subject of intense debate. Some researchers
believe that the entire injury develops during the ischemic period, whereas others argue that …

Abstract Objective: Mitochondrial [Ca2+]([Ca2+] m) rises in parallel with cytosolic
[Ca2+]([Ca2+] c) following ATP-depletion rigor contracture induced by hypoxia in isolated …