Autoimmune mediated G-protein receptor activation in cardiovascular and renal pathologies
Autoimmune mediated G-protein receptor activation in cardiovascular and renal pathologies
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DOI：
10.1160/th08-10-0710
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发表时间：
2009-04-01
影响因子：
6.7
通讯作者：
Hegner, Bjoern
中科院分区：
文献类型：
--
作者：
Dragun, Duska;Philippe, Aurelie;Hegner, Bjoern
针对 G 蛋白偶联受体 (GPCR) 的抗体可充当变构受体激动剂或拮抗剂。激动性抗体作用的典型疾病是甲状腺格雷夫斯病，50 年前首次描述了刺激 G 蛋白偶联促甲状腺激素受体 (TSHR) 的抗体。重症肌无力是拮抗性自身免疫作用的原型，其中针对烟碱乙酰胆碱受体（AChR）的抗体会导致神经肌肉接头阻断。抗体和 B 细胞越来越被认为是各种心血管和肾脏病理的主要调节剂。我们的目标是批判性地回顾针对其他 GPCR 的抗体可能放大或引起各种心血管和肾脏病理的概念，并总结当前的研究状况以及诊断和治疗策略的前景。在靶标方面，我们将重点关注α-肾上腺素能受体（α(1)AR）、β-肾上腺素能受体（β(1)AR）和血管紧张素II I型受体（AT(1)R）。
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 alpha-adrenergic receptor (alpha(1)AR), the beta-adrenergic receptor (beta(1)AR), and the angiotensin II type I receptor (AT(1)R).