Adrenergic regulation of myocardial apoptosis

Citation
K. Singh et al., Adrenergic regulation of myocardial apoptosis, CARDIO RES, 45(3), 2000, pp. 713-719
Citations number
51
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
CARDIOVASCULAR RESEARCH
ISSN journal
00086363 → ACNP
Volume
45
Issue
3
Year of publication
2000
Pages
713 - 719
Database
ISI
SICI code
0008-6363(200002)45:3<713:AROMA>2.0.ZU;2-Y
Abstract
Increased sympathetic nerve activity to the myocardium is a central feature in patients with heart failure. Norepinephrine, the primary transmitter of the sympathetic nervous system, signals via binding to alpha- and beta-adr energic receptors (AR) that are coupled to G-proteins. Pharmacologic studie s of cardiac myocytes in vitro demonstrate that P-AR can stimulate apoptosi s. Likewise, in transgenic mice overexpression of beta(1)-AR or Gas is asso ciated with myocyte apoptosis and the development of dilated cardiomyopathy . Whereas beta(1)-AR stimulate apoptosis in vitro and in vivo, beta(2)-AR m ay either stimulate or inhibit apoptosis and myocardial failure depending o n the level of expression. Receptors coupling to Gi and Gq may also be able to mediate or modulate apoptosis and the development of myocardial failure , suggesting the potential for interactions between the beta-AR system and numerous remodeling stimuli that act through Gi or Gq signaling pathways. I t appears likely that the mitogen-activated protein kinase superfamily play s a key role in mediating the actions of adrenergic pathways on myocyte apo ptosis. These observations suggest that the adrenergic nervous system plays an important role in the regulation of myocyte apoptosis, and may thus con tribute to the development of myocardial failure. (C) 2000 Elsevier Science B.V. All rights Reserved.