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The δA isoform of calmodulin kinase II mediates pathological cardiac hypertrophy by interfering with the HDAC4-MEF2 signaling pathway.

Abstract：

:Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) is a new promising target for prevention and treatment of cardiac hypertrophy and heart failure. There are three δ isoforms of CaMKII in the heart and previous studies focused primarily on δB and δC types. Here we report the δA isoform of CaMKII is also critically involved in cardiac hypertrophy. We found that δA was significantly upregulated in pathological cardiac hypertrophy in both neonatal and adult models. Upregulation of δA was accompanied by cell enlargement, sarcomere reorganization and reactivation of various hypertrophic cardiac genes including atrial natriuretic factor (ANF) and β-myocin heavy chain (β-MHC). Studies further indicated the pathological changes were largely blunted by silencing the δA gene and an underlying mechanism indicated selective interference with the HDAC4-MEF2 signaling pathway. These results provide new evidence for selective interfering cardiac hypertrophy and heart failure when CaMKII is considered as a therapeutic target.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Li C,Cai X,Sun H,Bai T,Zheng X,Zhou XW,Chen X,Gill DL,Li J,Tang XD

doi

10.1016/j.bbrc.2011.04.128

subject

Has Abstract

pub_date

2011-05-27 00:00:00

pages

125-30

issue

1

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(11)00735-2

journal_volume

409

pub_type

杂志文章

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