Abstract
Heart disease: recruitment of MEF2 activity by β-blockers wards off cardiomyocyte death.
Highlights
Morbidity and mortality associated with cardiovascular disease is a predominant global health problem
The initial cue that led to the inception of these studies was accumulating evidence in the central nervous system indicating that a primary function of MEF2 in neurons is to protect them from apoptosis.[4,5]
The striking connection was that the earlier work, in a skeletal muscle system, elucidated that Protein kinase A (PKA) phosphorylates the MEF2 protein complex enhancing its interaction with a co-repressor (HDAC4), inactivating MEF2 function.[7,8]
Summary
Morbidity and mortality associated with cardiovascular disease is a predominant global health problem. Death of cardiac muscle cells (cardiomyocytes) through programmed cell death (apoptosis) is one hallmark of the progression to heart failure.[1] loss of cardiomyocytes due to myocardial infarction (MI) in patients who survive the initial insult is a major determinant of residual heart function and their longer term prognosis.
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