Open AccessCa 2+ /Calmodulin-Dependent Protein Kinase II δ Mediates Myocardial Ischemia/Reperfusion Injury Through Nuclear Factor-κB
Author(s) -
Haiyun Ling,
Charles B.B. Gray,
Alexander C. Zambon,
Michael Grimm,
Yusu Gu,
Nancy D. Dalton,
Nicole H. Purcell,
Kirk L. Peterson,
Joan Heller Brown
Publication year - 2013
Publication title -
circulation research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.899
H-Index - 336
eISSN - 1524-4571
pISSN - 0009-7330
DOI - 10.1161/circresaha.112.276915
Subject(s) - kinase , in vivo , knockout mouse , reperfusion injury , inflammation , downregulation and upregulation , iκbα , phosphorylation , ischemia , chemistry , protein kinase a , microbiology and biotechnology , endocrinology , medicine , nf κb , biology , biochemistry , receptor , gene
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.
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