New Perspectives in cAMP-Signaling Modulation |
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Authors: | Magali Berthouze Anne-Coline Laurent Magali Breckler Frank Lezoualc��h |
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Institution: | INSERM, UMR-1048, Institut des Maladies Métaboliques et Cardiovasculaires, 1 Avenue Jean Poulhès, BP 84225, 31342, Toulouse Cedex 4, France. |
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Abstract: | Cyclic adenosine 3′,5′-monophosphate (cAMP) mediates the biological effects of various hormones and neurotransmitters. Stimulation
of cardiac β-adrenergic receptors (β-AR) via catecholamines leads to activation of adenylyl cyclases and increases cAMP production
to enhance myocardial function. Because many other receptors signaling through cAMP generation exist in cardiac myocytes,
a central question is how different hormones induce distinct cellular responses through the same second messenger. A large
body of evidence suggests that the localization and compartmentalization of β-AR/cAMP signaling affects the net outcome of
biological functions. Spatiotemporal dynamics of cAMP action is achieved by various proteins, including protein kinase A (PKA),
phosphodiesterases, and scaffolding proteins such as A-kinase–anchoring proteins. In addition, the discovery of the cAMP target
Epac (exchange proteins directly activated by cAMP), which functions in a PKA-independent manner, represents a novel mechanism
for governing cAMP-signaling specificity. Aberrant cAMP signaling through dysregulation of β-AR/cAMP compartmentalization
may contribute to cardiac remodeling and heart failure. |
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