β-Adrenergic Receptor-Stimulated Cardiac Myocyte Apoptosis : Role of β1 Integrins

Abstract EN

Increased sympathetic nerve activity to the myocardium is a central feature in patients with heart failure.

Accumulation of catecholamines plays an important role in the pathogenesis of heart disease.

Acting via β-adrenergic receptors (β-AR), catecholamines (norepinephrine and isoproterenol) increase cardiac myocyte apoptosis in vitro and in vivo.

Specifically, β1-AR and β2-AR coupled to Gαs exert a proapoptotic action, while β2-AR coupled to Gi exerts an antiapoptotic action.

β1 integrin signaling protects cardiac myocytes against β-AR-stimulated apoptosis in vitro and in vivo.

Interaction of matrix metalloproteinase-2 (MMP-2) with β1 integrins interferes with the survival signals initiated by β1 integrins.

This paper will discuss background information on β-AR and integrin signaling and summarize the role of β1 integrins in β-AR-stimulated cardiac myocyte apoptosis.