Jahns Roland, Boivin Valérie, Lohse Martin J
Department of Internal Medicine, Medizinische Klinik und Poliklinik I, University of Würzburg, D-97080 Würzburg, Germany.
Trends Cardiovasc Med. 2006 Jan;16(1):20-4. doi: 10.1016/j.tcm.2005.11.002.
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.
扩张型心肌病(DCM)是一种心脏病,其特征是心功能进行性衰退以及左心室扩张,病因不明且无冠状动脉疾病。遗传因素和心脏毒性物质约占DCM病例的三分之一,但其余60%至70%的病因仍不清楚。在过去二十年中,越来越多的证据表明,靶向心脏β1 - 肾上腺素能受体的功能性活性抗体或自身抗体(抗β1 - AR抗体)可能在DCM的发病和/或临床过程中起重要作用。最近在大鼠身上进行的实验表明,此类抗体实际上可导致DCM。本文综述了当前的知识以及最近的实验和临床研究结果,重点关注β1 - 肾上腺素能受体作为自身抗原在DCM发病机制中的作用。