IMR Press / FBL / Volume 14 / Issue 5 / DOI: 10.2741/3334

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
Pathogenesis and therapy of autoimmunity-induced dilated cardiomyopathy
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1 Department of Cardiology, Shandong Provincial Hospital, Shandong University, Jinan, Shandong 250021, Cihina
2 Center for Cardiovascular Research and Alternative Medicine, University of Wyoming, Laramie, WY 82071, USA
3 Department of Biomedical Sciences, Baylor College of Dentistry, Texas A&M Health Science Center, Dallas, TX 75246, USA
Academic Editor:Avadhesh Sharma
Front. Biosci. (Landmark Ed) 2009, 14(5), 1708–1715;
Published: 1 January 2009
(This article belongs to the Special Issue Advances in systemic inflammatory response)

Myocarditis and dilated cardiomyopathy can potentially originate from autoimmune responses. Although genetic predisposition, viral infection, molecular mimicry, and oxidative stress are potential contributing factors to dilated cardiomyopathy, the underlying mechanism (s) has not been fully elucidated. Autoantibodies (AABs) against cardiotropic targets such as β-adrenergic receptors, mitochondria proteins, myosin, tropomyocin and actin as well as structural proteins such as laminin and desmin may participate in the development of dilated cardiomyopathy. These autoantibodies disrupt cardiac excitation-contraction coupling and activate immune response to initiate tissue injury through complement and circulatory immunocomplexes (CICs). These antibodies are present prior to the onset of dilated cardiomyopathy and may be used to predict the deterioration of cardiac function. Depletion of these cardiac-specific antibodies by extracorporeal immunoabsorption has been considered as a new and effective approach in the treatment of autoimmunity-induced dilated cardiomyopathy. In order to better understand the pathogenesis and therapeutic remedy against this myopathy, the present review will summarize the manifestation and key signaling mechanisms involved in compromised cardiac contractile function during autoimmunity.

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