beta(1)-Adrenergic receptor function, autoimmunity, and pathogenesis
of dilated cardiomyopathy
R. Jahns, V. Boivin, and M. Lohse. Trends Cardiovasc Med, 16 (1):
20-4(January 2006)Jahns, Roland Boivin, Valerie Lohse, Martin J Research Support, Non-U.S.
Gov't Review United States Trends in cardiovascular medicine Trends
Cardiovasc Med. 2006 Jan;16(1):20-4..
Abstract
Dilated cardiomyopathy (DCM) is a heart disease characterized by progressive
depression of cardiac function and left ventricular dilatation of
unknown etiology in the absence of coronary artery disease. Genetic
causes and cardiotoxic substances account for about one third of
the DCM cases, but the etiology of the remaining 60% to 70% is still
unclear. Over the past two decades, evidence has accumulated continuously
that functionally active antibodies or autoantibodies targeting cardiac
beta(1)-adrenergic receptors (anti-beta(1)-AR antibodies) may play
an important role in the initiation and/or clinical course of DCM.
Recent experiments in rats indicate that such antibodies can actually
cause DCM. This article reviews current knowledge and recent experimental
and clinical findings focusing on the role of the beta(1)-adrenergic
receptor as a self-antigen in the pathogenesis of DCM.
Jahns, Roland Boivin, Valerie Lohse, Martin J Research Support, Non-U.S.
Gov't Review United States Trends in cardiovascular medicine Trends
Cardiovasc Med. 2006 Jan;16(1):20-4.
%0 Journal Article
%1 Jahns2006a
%A Jahns, R.
%A Boivin, V.
%A Lohse, M. J.
%D 2006
%J Trends Cardiovasc Med
%K *Autoimmunity Animals Autoantibodies/*biosynthesis/blood/physiology Cardiomyopathy, Dilated/*etiology/immunology/physiopathology Humans beta-1/*immunology/physiology Receptor Adrenergic
%N 1
%P 20-4
%T beta(1)-Adrenergic receptor function, autoimmunity, and pathogenesis
of dilated cardiomyopathy
%U http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16387626
%V 16
%X Dilated cardiomyopathy (DCM) is a heart disease characterized by progressive
depression of cardiac function and left ventricular dilatation of
unknown etiology in the absence of coronary artery disease. Genetic
causes and cardiotoxic substances account for about one third of
the DCM cases, but the etiology of the remaining 60% to 70% is still
unclear. Over the past two decades, evidence has accumulated continuously
that functionally active antibodies or autoantibodies targeting cardiac
beta(1)-adrenergic receptors (anti-beta(1)-AR antibodies) may play
an important role in the initiation and/or clinical course of DCM.
Recent experiments in rats indicate that such antibodies can actually
cause DCM. This article reviews current knowledge and recent experimental
and clinical findings focusing on the role of the beta(1)-adrenergic
receptor as a self-antigen in the pathogenesis of DCM.
@article{Jahns2006a,
abstract = {Dilated cardiomyopathy (DCM) is a heart disease characterized by progressive
depression of cardiac function and left ventricular dilatation of
unknown etiology in the absence of coronary artery disease. Genetic
causes and cardiotoxic substances account for about one third of
the DCM cases, but the etiology of the remaining 60% to 70% is still
unclear. Over the past two decades, evidence has accumulated continuously
that functionally active antibodies or autoantibodies targeting cardiac
beta(1)-adrenergic receptors (anti-beta(1)-AR antibodies) may play
an important role in the initiation and/or clinical course of DCM.
Recent experiments in rats indicate that such antibodies can actually
cause DCM. This article reviews current knowledge and recent experimental
and clinical findings focusing on the role of the beta(1)-adrenergic
receptor as a self-antigen in the pathogenesis of DCM.},
added-at = {2010-12-14T18:12:02.000+0100},
author = {Jahns, R. and Boivin, V. and Lohse, M. J.},
biburl = {https://www.bibsonomy.org/bibtex/27f4a426a0dc620b441d0d4fd0fe6a7f3/pharmawuerz},
endnotereftype = {Journal Article},
interhash = {2a2981d9550c31eb4c42091ee41ab9c8},
intrahash = {7f4a426a0dc620b441d0d4fd0fe6a7f3},
issn = {1050-1738 (Print) 1050-1738 (Linking)},
journal = {Trends Cardiovasc Med},
keywords = {*Autoimmunity Animals Autoantibodies/*biosynthesis/blood/physiology Cardiomyopathy, Dilated/*etiology/immunology/physiopathology Humans beta-1/*immunology/physiology Receptor Adrenergic},
month = Jan,
note = {Jahns, Roland Boivin, Valerie Lohse, Martin J Research Support, Non-U.S.
Gov't Review United States Trends in cardiovascular medicine Trends
Cardiovasc Med. 2006 Jan;16(1):20-4.},
number = 1,
pages = {20-4},
shorttitle = {beta(1)-Adrenergic receptor function, autoimmunity, and pathogenesis
of dilated cardiomyopathy},
timestamp = {2010-12-14T18:22:40.000+0100},
title = {beta(1)-Adrenergic receptor function, autoimmunity, and pathogenesis
of dilated cardiomyopathy},
url = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16387626},
volume = 16,
year = 2006
}