Department of Internal Medicine, Section of Cardiovascular Medicine, Yale School of Medicine, Cardiovascular Research Center, 300 George Street, Rm 759H, New Haven, CT 06511, USA.
Curr Mol Med. 2011 Oct;11(7):517-28. doi: 10.2174/156652411800615144.
The prostacyclin receptor (IP--International Union of Pharmacology nomenclature) is a member of the seven transmembrane G-protein coupled receptor (GPCR) superfamily. Recent concerns with selective and non-selective COX-1/COX-2 inhibition have exposed an important cardioprotective role for IP in preventing atherothrombosis. Receptor dysfunction (genetic variants) or reduced signaling (COX-2 inhibition) in high cardiovascular risk patients leads to increased cardiovascular events. These clinical observations have also been confirmed genetically by mouse knockout studies. Thus, receptor regulation is paramount in ensuring correct function in the prevention of atherothrombosis. This review summarizes recent literature on how this important receptor is regulated, from transcription to transport (to and from the membrane surface). These regulatory processes are critical in ensuring that IP receptors are adequately expressed and functional on the cell surface.
前列环素受体（国际药理学联合会命名）是七跨膜 G 蛋白偶联受体（GPCR）超家族的成员。最近对选择性和非选择性 COX-1/COX-2 抑制的关注，揭示了 IP 在预防动脉血栓形成方面的重要心脏保护作用。在心血管风险高的患者中，受体功能障碍（遗传变异）或信号转导减少（COX-2 抑制）会导致心血管事件增加。这些临床观察结果也通过小鼠基因敲除研究得到了证实。因此，受体调节对于确保在预防动脉血栓形成方面的正确功能至关重要。本综述总结了最近关于该重要受体如何被调节的文献，从转录到运输（到膜表面和从膜表面）。这些调节过程对于确保 IP 受体在细胞表面得到充分表达和功能至关重要。
