Abstract During ischemia/reperfusion (IR), increased activation of angiotensin AT 1
receptors recruits NADPH oxidase 2 (NOX2) which contributes to oxidative stress. It is …

Reactive oxygen species (ROS) contribute to myocardial death during ischemia-reperfusion
(I/R) injury, but detailed knowledge of molecular pathways connecting ROS to cardiac injury …

Abstract Deletion of Ca 2+/calmodulin-dependent protein kinase II delta (CaMKIIδ) has been
shown to protect against in vivo ischemia/reperfusion (I/R) injury. It remains unclear which …

Abstract Objectives: Ca2+/calmodulin-dependent protein kinase II (CaMKII) has been
implicated in the regulation of cardiac excitation–contraction coupling (ECC) as well as in …

Content of particular proteins indicating cellular injury due to apoptosis and necrosis has
been investigated in ischemic/reperfused (IR) hearts and ischemic/reperfused hearts treated …

Myocardial infarction and revascularization cause cardiac ischemia/reperfusion (I/R) injury
featuring cardiomyocyte death and inflammation. The Ca 2+/calmodulin dependent protein …

OBJECTIVE: To investigate the role of calcium/calmodulin-dependent protein kinase II
(CaMKII) in myocardial ischemia-reperfusion (IR) injury in isolated perfused rat heart and …

Background: CaMKII (Ca2+/calmodulin-dependent kinase II) plays a central role in cardiac
ischemia/reperfusion (I/R) injury—an important therapeutic target for ischemic heart disease …

Excessive activation of the β-adrenergic, angiotensin II (Ang II) and aldosterone signaling
pathways promotes mortality after myocardial infarction, and antagonists targeting these …

Rationale: Ca2+/calmodulin-dependent protein kinase II (CaMKII) has been implicated as a
maladaptive mediator of cardiac ischemic injury. We hypothesized that the inflammatory …