Ca2+/Calmodulin-dependent protein kinase II δ mediates myocardial ischemia/reperfusion injury through nuclear factor-κB.

ABSTRACT:

Rationale

Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) has been implicated as a maladaptive mediator of cardiac ischemic injury. We hypothesized that the inflammatory response associated with in vivo ischemia/reperfusion (I/R) is initiated through CaMKII signaling.

Objective

To assess the contribution of CaMKIIδ to the development of inflammation, infarct, and ventricular dysfunction after in vivo I/R and define early cardiomyocyte-autonomous events regulated by CaMKIIδ using cardiac-specific knockout mice.

Methods and results

Wild-type and CaMKIIδ knockout mice were subjected to in vivo I/R by occlusion of the left anterior descending artery for 1 hour followed by reperfusion for various times. CaMKIIδ deletion protected the heart against I/R damage as evid

SUBMITTER: Ling H 

PROVIDER: S-EPMC3673710 | biostudies-literature | 2013 Mar

REPOSITORIES: biostudies-literature