Inhibition of p38 mitogen-activated protein kinase protects the heart against cardiac remodeling in mice with heart failure resulting from myocardial infarction
BACKGROUND: Mitogen-activated protein kinases (MAPKs) have emerged as an important
pathophysiologic regulator during the development of heart failure (HF). p38 MAPK activity
is elevated in cardiac hypertrophy and HF. We used a mouse model of myocardial infarction
(MI) to test the hypotheses that (1) inhibition of p38 MAPK activity may improve cardiac
function and remodeling after myocardial infarction (MI) and (2) coadministration of a p38
inhibitor (p38i) and an angiotensin-converting enzyme inhibitor (ACEI) may provide only …
pathophysiologic regulator during the development of heart failure (HF). p38 MAPK activity
is elevated in cardiac hypertrophy and HF. We used a mouse model of myocardial infarction
(MI) to test the hypotheses that (1) inhibition of p38 MAPK activity may improve cardiac
function and remodeling after myocardial infarction (MI) and (2) coadministration of a p38
inhibitor (p38i) and an angiotensin-converting enzyme inhibitor (ACEI) may provide only …
