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.
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