Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular Research Institute of Wuhan University, Hubei Key Laboratory of Cardiology, Jiefang Road 238, Wuchang, 430060 Wuhan, P.R. China.
Biosci Rep. 2021 Jan 29;41(1). doi: 10.1042/BSR20203387.
Ghrelin, a 28-aminoacid peptide, was isolated from the human and rat stomach and identified in 1999 as an endogenous ligand for the growth hormone secretagogue-receptor (GHS-R). In addition to stimulating appetite and regulating energy balance, ghrelin and its receptor GHS-R1a have a direct effect on the cardiovascular system. In recent years, it has been shown that ghrelin exerts cardioprotective effects, including the modulation of sympathetic activity and hypertension, enhancement of the vascular activity and angiogenesis, inhibition of arrhythmias, reduction in heart failure and inhibition of cardiac remodeling after myocardial infarction (MI). The cardiovascular protective effect of ghrelin may be associated with anti-inflammation, anti-apoptosis, inhibited sympathetic nerve activation, regulated autophagy, and endothelial dysfunction. However, the molecular mechanisms underlying the effects of ghrelin on the cardiovascular system have not been fully elucidated, and no specific therapeutic agent has been established. It is important to further explore the pharmacological potential of ghrelin pathway modulation for the treatment of cardiovascular diseases.
胃饥饿素是一种 28 个氨基酸的肽,最初从人类和大鼠的胃中分离出来,并于 1999 年被鉴定为生长激素促分泌素受体(GHS-R)的内源性配体。除了刺激食欲和调节能量平衡外,胃饥饿素及其受体 GHS-R1a 对心血管系统有直接影响。近年来,研究表明胃饥饿素具有心脏保护作用,包括调节交感神经活动和高血压、增强血管活性和血管生成、抑制心律失常、减少心力衰竭以及抑制心肌梗死后的心脏重构。胃饥饿素的心血管保护作用可能与抗炎、抗细胞凋亡、抑制交感神经激活、调节自噬和内皮功能障碍有关。然而,胃饥饿素对心血管系统影响的分子机制尚未完全阐明,也没有确立特定的治疗药物。因此,进一步探索胃饥饿素途径调节的药理学潜力,对于治疗心血管疾病非常重要。