IMR Press / FBL / Volume 23 / Issue 11 / DOI: 10.2741/4695

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.


Relevant effects of beta1-adrenoceptor autoantibodies in chronic heart failure

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1 Institute for Pharmacology and Toxicology, University of Wuerzburg, Germany
2 Comprehensive Heart Failure Center (CHFC), University and University Hospital of Wuerzburg, Germany
3 Interdisciplinary Bank of Biomaterials and Data Wuerzburg (IBDW), University and University Hospital of Wuerzburg, Germany
4 Institute of Clinical Chemistry and Laboratory Diagnostics, University and University Hospital, Duesseldorf, Germany
Front. Biosci. (Landmark Ed) 2018, 23(11), 2146–2156;
Published: 1 June 2018

Patients suffering from chronic heart failure (CHF) caused or promoted by autoantibodies against cardiac β1-adrenergic receptors (β1AR) could benefit from specific therapies aimed at tolerance induction, removal or neutralisation of β1AR autoantibodies, provided the patients can be selected for these therapies by reliable detection and quantitation of β1AR autoantibodies in their circulation and by a valid assessment of the autoantibodies’s putative cardio-pathogenic potential. Here, we discuss the current state of knowledge regarding the effects of CHF-associated (auto)antibodies on β1AR function and β1AR-mediated signal tranduction and discuss the presumed role of these effects in the development and progression of CHF. Identification of disease-relevant functional autoantibody effects and their specific assessment in medical diagnostic will be a prerequesite for the implementation of novel specific therapies not only for CHF caused or promoted by β1AR autoantibodies but alos for most other diseases involving autoantibodies that target G-protein coupled receptors.

Chronic Heart Failure
Beta1-Adrenergic Receptor
Signal Transduction
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