IMR Press / FBL / Volume 23 / Issue 11 / DOI: 10.2741/4690

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.


GPCR-autoantibodies in chronic heart failure

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1 Institute of Pharmacology and Toxicology, University of Wuerzburg, Versbacher Str. 9, 97078 Wuerzburg, Germany
2 Comprehensive Heart Failure Center (CHFC), University Hospital of Wuerzburg, Am Schwarzenberg 15, 97078 Wuerzburg, Germany
3 Interdisciplinary Bank of Biomaterials and Data Wuerzburg (IBDW), University Hospital of Wuerzburg, Straubmuehlweg 2a, 97078 Wuerzburg, Germany
Front. Biosci. (Landmark Ed) 2018, 23(11), 2065–2081;
Published: 1 June 2018

Chronic heart failure (CHF) is a syndrome characterized by shortness of breath, fluid retention, and a progressive reduction in cardiac function. More than 60% of the cases are ischemic in origin (i.e., due to myocardial infarction) and about 30% are caused by non-ischemic myocardial damage (i.e., due to genetic or non-genetic causes like myocardial inflammation). Because of alterations in both cellular and humoral immunity patients with non-ischemic CHF often develop abnormal or misled immune responses, including cross-reacting antibodies and/or autoantibodies to various cardiac antigens. Non-ischemic myocardial damage was found to progress to CHF particularly, when associated (a) with the generation of autoantibodies directed against distinct myocyte membrane proteins critically involved in cardiac function – like G-protein coupled membrane receptors (GPCRs), or (b) with virus persistence in the myocardium. This article will review current knowledge on the pathophysiological relevance of GPCR-autoreactivity in CHF by giving an overview on the so far available evidence from pre-clinical, clinical and epidemiological studies on the CHF-inducing potential of GPCR-autoantibodies and thereon based novel therapeutic approaches in GPCR autoantibody-associated CHF.

Beta1-adrenergic receptor
G protein-coupled receptors
Heart Failure
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