Does gadd45γ regulate cardiomyocyte death and post-myocardial infarction left ventricular remodelling?
This work is the first to demonstrate that Gadd45γ accumulation during MI promotes the development and persistence of HF by inducing cardiomyocyte apoptosis in a p38 MAPK-dependent manner. We clearly identify Gadd45γ as a therapeutic target in the development of HF.
Longitudinal global mean strain provides improved early prediction of infarct size in patients with AMI compared with longitudinal global strain and left ventricular ejection fraction.