儿茶酚抑素(catestatin)是一种由嗜铬粒蛋白A 衍生的多功能神经内分泌肽, 广泛表达于神经、内分泌、免疫和心血管系统。儿茶酚抑素可与烟碱型乙酰胆碱受体结合, 激活磷脂酰肌醇3-激酶/蛋白激酶B(phosphatidylinositol 3-kinase/protein kinase B, PI3K/Akt)、丝裂原活化蛋白激酶/细胞外信号调节激酶(mitogen-activated protein kinase/extracellular signal-regulated kinase, MAPK/ERK)、Toll样受体4 /p38丝裂原活化蛋白激酶(toll-like receptor 4/p38 mitogen-activated protein kinase, TLR4/p38 MAPK)、Notch1信号通路,具有抗氧化、促进血管生成、调控免疫稳态、调节糖脂代谢等多种生物学效应。近期研究表明,儿茶酚抑素参与高血压、动脉粥样硬化、炎症性肠病、糖尿病、先兆子痫等多种疾病的病生理过程。本文就儿茶酚抑素的来源、结构、受体及相关的信号通路、生物学效应及病理生理意义的研究新进展做简要综述, 以期为儿茶酚抑素的机制研究与临床应用提供系统性理论依据。

Catestatin, a multifunctional neuroendocrine peptide derived from chromogranin A, is widely expressed in the nervous, endocrine, immune, and cardiovascular systems. Catestatin can bind to nicotinic acetylcholine receptors, activating the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt),mitogen-activated protein kinase/extracellular signal-regulated kinase(MAPK/ERK), toll-like receptor 4/p38 mitogen-activated protein kinase (TLR4/p38 MAPK), and Notch1 signaling pathways, exerting various biological effects such as antioxidation, promotion of angiogenesis, regulation of immune homeostasis, and modulation of glucose and lipid metabolism. Recent studies have shown that catestatin is involved in the pathophysiological processes of several diseases, including hypertension, atherosclerosis, inflammatory bowel disease, diabetes, and preeclampsia. This review focuses on recent research progress on the origin, structure, receptors, associated signaling pathways, biological effects, and pathophysiological significance of catestatin, with the aim of providing a theoretical basis for further mechanistic research and potential clinical applications of catestatin.