Long Non-Coding RNA Malat-1 Is Dispensable during Pressure Overload-Induced Cardiac Remodeling and Failure in Mice.

The preoperative muscle dysfunction, verified by maximal inspiratory pressure in patients with heart failure undergoing cardiac surgery does not appear to influence the incidence

In the trained animals, the inhibition of NO synthesis attenuated hypertension, induced cardiac hypertrophy and significantly increased myocardial fibrosis, indicating that NO plays

To evaluate the impact of compound 1 in CVB3- induced myocarditis, body weight, heart rate (HR), maximum left ventricle pressure (Pmax), maximum left ventricle pressure rise

and in the heart, are induced and function during muscle differentiation (7). However, several open questions remain regarding miRNAs and their role in cardiac hypertrophy. 1) What

In conclusion, RT prevented interstitial collagen deposition in LV rats subjected to 1% NaCl and attenuated diastolic dysfunction induced by salt overload independent of alterations

investigate in a experimental model of volume overload cardiac hypertrophy: 1) whether or not there is increased car- diac collagen accumulation, 2) the dis- tribution and type

To gain insight into the relevance of de novo CpG methylation in cardiac hypertrophy and failure, we subjected these mice to left ventricular pressure overload by transverse

Skeletal and cardiac muscle fibrosis were also significantly increased in untreated mdx mice compared to wild type, but there was no significant improvement in treated mdx mice..