G蛋白偶联受体30的特点及其在纤维化疾病中的作用机制

Characteristics of G-protein-coupled receptor 30 and its mechanism in fibrotic diseases

纤维化是一种组织受到破坏后的修复反应,主要由于炎症因子过度刺激引发实质细胞坏死、细胞外基质(extracellular matrix,ECM)分泌过剩,大量沉积于细胞间质,形成胶原蛋白排列紊乱的病理表现,严重者导致器官结构紊乱和功能障碍,甚至发生器官衰竭[1]。据报道,纤维化是一种不可逆的病理过程[2],目前临床上对纤维化疾病以干预和对症治疗为主[3],尚无特定的治疗药物。肿瘤坏死因子α(tumor necrosis factor-α,TNF-α)和白细胞介素1β(interleukin-1β,IL-1β)[4-5]已被确定为多种纤维化疾病治疗的关键靶点。那么,阻断炎症因子的信号途径是否可控制纤维化的发生、发展?G蛋白偶联受体30(G-protein-coupled receptor 30,GPR30)是一种7次跨膜雌激素受体蛋白。

Fibrotic lesions of all organs show similar histological abnormalities such as decreased parenchymal cells and increased interstitial fibrous connective tissue. Fibrotic lesions may lead to structural abnormalities and functional disorders of organs,and even organ failure. Inflammatory response is the initiating factor of the occurrence and development of fibrotic diseases. Activation of G-protein-coupled receptor 30(GPR30)can exert the anti-inflammatory effect,but the mechanism of GPR30 in fibrotic diseases is still unclear. Here we reviewed the research progress of GPR30 in regulating myocardial fibrosis,liver fibrosis and renal fibrosis.