Thromb Haemost 2009; 101(04): 643-648
DOI: 10.1160/TH08-10-0710
Theme Issue Article
Schattauer GmbH

Autoimmune mediated G-protein receptor activation in cardiovascular and renal pathologies

Duska Dragun
1   Department of Nephrology and Intensive Care Medicine Campus Virchow-Klinikum and Center for Cardiovascular Research Medical Faculty of the Charité Berlin, Berlin, Germany
,
Aurélie Philippe
1   Department of Nephrology and Intensive Care Medicine Campus Virchow-Klinikum and Center for Cardiovascular Research Medical Faculty of the Charité Berlin, Berlin, Germany
,
Rusan Catar
1   Department of Nephrology and Intensive Care Medicine Campus Virchow-Klinikum and Center for Cardiovascular Research Medical Faculty of the Charité Berlin, Berlin, Germany
,
Björn Hegner
1   Department of Nephrology and Intensive Care Medicine Campus Virchow-Klinikum and Center for Cardiovascular Research Medical Faculty of the Charité Berlin, Berlin, Germany
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Publikationsverlauf

Received: 03. November 2008

Accepted after minor revision: 31. März 2008

Publikationsdatum:
23. November 2017 (online)

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Summary

Antibodies directed against G-protein coupled receptors (GPCR) can act as allosteric receptor agonists or antagonists. Prototypic disease for agonistic antibody action is a Graves disease of the thyroid gland where antibodies that stimulate G-protein coupled thyroid-stimulating hormone receptor (TSHR) were first described 50 years ago. Myasthenia gravis is the prototype for antagonistic autoimmune actions, where antibodies directed against the nicotinic acetylcholine receptor (AChR) cause blockade of neuromuscular junctions. Antibodies and B-cells are increasingly recognised as major modulators of various cardiovascular and renal pathologies. We aim to critically review the notion that antibodies targeting other GPCRs may amplify or cause various cardiovascular and renal pathologies and summarise the current state of research, as well as perspectives in diagnostic and therapeutic strategies. In terms of targets we will focus on the α-adrenergic receptor (α1AR), the β-adrenergic receptor (β1AR), and the angiotensin II type 1 receptor (AT1R).