Targeted Deletion of the Extracellular Signal-Regulated Protein Kinase 5 Attenuates Hypertrophic Response and Promotes Pressure Overload—Induced Apoptosis in the Heart.

The article examines the in vivo role and signaling mechanism of extracellular signal-regulated protein kinase (ERK)5 in regulating hypertrophy-induced apoptosis and cardiac hypertrophy in mice. Study demonstrates the increased apoptosis and upregulated p53 expression levels. It shows the significant function of ERK5 in cardiomyocyte survival and cardiac hypertrophic remodeling. Its role in hypertrophic remodeling can be mediated through myocyte enhancer factor (MEF)2 activity.