Abstract
enlargement, increased incidence of thrombi, fibrosis and increased atrial natriuretic peptide. Each of these parameters was significantly blunted/improved in LNAantimiR-34 treated TACmice. Cardiac function (fractional shortening) improved by 14% with treatment (n= 9, p< 0.001). Furthermore, -myosin heavy chain (MHC)/ MHC and sarcoplasmic reticulum Ca2+ ATPase gene expression were significantly increased in antimiR-34 treated TAC mice. Conclusion: Administration of antimiR-34 in a mouse model of pressure overload attenuated pathological remodelling and improved cardiac function. Targeting PI3K-regulatedmiRsmay be a therapeutic strategy for the treatment of heart failure. http://dx.doi.org/10.1016/j.hlc.2012.05.012
Published Version
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