Targeted inhibition of p38 MAPK promotes hypertrophic cardiomyopathy through upregulation of calcineurin-NFAT signaling

Cardiac-specific transgenic mice expressing dominant-negative mutants of p38α, MKK3, or MKK6, and NFAT-dependent luciferase reporter transgenic mice

Targeted inhibition of p38 MAPK via dominant-negative mutants, combined with hypertrophic stimuli (aortic banding, Ang II infusion, isoproterenol infusion, or phenylephrine infusion for 14 days) or genetic disruption of calcineurin Aβ gene

Cardiac hypertrophy and myopathysurrogate