Reperfusion is mandatory to salvage ischemic myocardium from infarction, but reperfusion
per se contributes to injury and ultimate infarct size. Therefore, cardioprotection beyond that …

Mitochondria play an important role in cell death and cardioprotection. During ischemia,
when ATP is progressively depleted, ion pumps cannot function resulting in a rise in calcium …

Yellon, Derek M., and James M. Downey. Preconditioning the Myocardium: From Cellular
Physiology to Clinical Cardiology. Physiol Rev 83: 1113-1151, 2003; 10.1152/physrev …

Despite nearly twenty years of research into the field of ischemic preconditioning, the actual
mechanism of protection remains unclear. However, much progress has been made in …

Myocardial ischemia and ischemia/reperfusion activate several protein kinase pathways.
Protein kinase activation potentially regulates the onset of myocardial cell injury and the …

MAPK activities, including JNK, p38, and ERK, are markedly enhanced after ischemia in
vivoand chemical anoxia in vitro. The relative extent of JNK, p38, or ERK activation has been …

It has been assumed that all Gi-coupled receptors trigger the protective action of
preconditioning by means of an identical intracellular signaling pathway. To test this …

In this article, we review the literature regarding the role of c-Jun N-terminal kinases (JNKs)
in cerebral and myocardial ischemia/reperfusion injury. Numerous studies demonstrate that …

Reactive oxygen species (ROS) participate in cardioprotection of ischemic reperfusion (I/R)
injury via preconditioning mechanisms. Mitochondrial ROS have been shown to play a key …

Adenosine (Ado) accumulates in tissues under metabolic stress. On myocardial cells, the
nucleoside interacts with various receptor subtypes (A1, A3, and probably A2A and A2B) …