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Death, Cardiac Dysfunction, and Arrhythmias Are Increased by Calmodulin Kinase II in Calcineurin Cardiomyopathy
Author(s) -
Michelle S.C. Khoo,
Jingdong Li,
Madhu V. Singh,
Yingbo Yang,
Prince J. Kannankeril,
Yuejin Wu,
Chad E. Grueter,
Xiaoqun Guan,
Carmine V. Oddis,
Rong Zhang,
Lisa A. Mendes,
Gemin Ni,
Ernest C. Madu,
Jinying Yang,
Martha A. Bass,
Rey J. Gomez,
Brian E. Wadzinski,
Eric N. Olson,
Roger Colbran,
Mark E. Anderson
Publication year - 2006
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.106.644583
Subject(s) - calcineurin , genetically modified mouse , transgene , medicine , cardiomyopathy , endocrinology , calmodulin , nfat , cardiac function curve , sudden death , phosphatase , heart failure , microbiology and biotechnology , biology , phosphorylation , transplantation , calcium , biochemistry , gene
Activation of cellular Ca2+ signaling molecules appears to be a fundamental step in the progression of cardiomyopathy and arrhythmias. Myocardial overexpression of the constitutively active Ca2+-dependent phosphatase calcineurin (CAN) causes severe cardiomyopathy marked by left ventricular (LV) dysfunction, arrhythmias, and increased mortality rate, but CAN antagonist drugs primarily reduce hypertrophy without improving LV function or risk of death.

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