Gastrin signaling in cardiovascular pathophysiology: From molecular crosstalk to clinical implications.

As a gastrointestinal hormone, gastrin stimulates gastric acid secretion and intestinal mucosal nutrition. Evidence links it closely to coronary heart disease, ischemia‒reperfusion injury and hypertension. The relevant literature was systematically retrieved from PubMed, Web of Science, China National Knowledge Infrastructure (CNKI), and other scientific databases, as well as other sources. Gastrin is a polypeptide hormone that is synthesized mainly by G cells in the antrum and proximal small intestine. Its secretion is controlled by neural regulation and humoral regulation. Gastrin is significantly associated with coronary heart disease, cardiac ischemia-reperfusion injury, hypertension and other cardiovascular diseases. The risk of coronary heart disease in patients with high serum gastrin levels is greater than that in the general population, and the serum gastrin level is higher in patients with myocardial infarction, which further suggests that hypergastrinemia may be an important risk factor for CHD. Myocardial cells express CCKBR, and intracoronary gastrin administration improves myocardial contractility through CCKBR. Several studies have shown that gastrin can also protect the myocardium against ischemia-reperfusion injury through the STAT3 signaling pathway. Gastrin may regulate blood pressure through the central nervous system or directly dilate blood vessels. Gastrin can promote the secretion of gastric acid and nutrition of intestinal mucosa. Gastrin exerts cardioprotective effects and regulates the occurrence of hypertension.