MGP翻译后修饰及其抑制血管钙化分子机制的研究进展  

Progress in post-translational modification and molecular mechanism of MGP as a vascular calcification inhibitor

作　　者：洪敏雯 李清峰 刘康 梁丹 李世新 郝振宇 HONG Minwen;LI Qingfeng;LIU Kang;LIANG Dan;LI Shixin;HAO Zhenyu(College of Bioscience and Biotechnology,Yangzhou University,Yangzhou 225009,China;Affiliated Hospital of Yangzhou University,Yangzhou 225009,China)

机构地区：[1]扬州大学生物科学与技术学院,江苏扬州225009 [2]扬州大学附属医院,江苏扬州225009

出　　处：《中国病理生理杂志》2024年第12期2359-2366,共8页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助项目(No.82370136);江苏省自然科学基金资助项目(No.BK20210828,No.BK20231333);江苏省特聘教授资助项目;江苏省高等学校自然科学基金面上项目(No.21KJB610002);中国博士后科学基金面上项目(No.2023M732983)。

摘　　要：基质γ-羧基谷氨酸蛋白(matrix gamma-carboxyglutamate protein, MGP)作为一种维生素K依赖性蛋白,是天然存在的血管钙化抑制蛋白。MGP的钙化抑制功能与其翻译后修饰紧密相关,特别是γ-谷氨酰羧化修饰和磷酸化修饰。但囿于其极低的溶解度和相对复杂的翻译后修饰,MGP抑制血管钙化的分子机制仍不清晰。在此,本文总结了目前有关MGP翻译后修饰与钙化抑制机制研究方面的进展和争论,阐述了由于MGP功能缺陷所引起的心脑血管疾病、慢性肾病和Keutel综合症等疾病的研究现状。希望本文能够促进我们对于MGP抑制血管钙化分子机制的理解,并有助于开发因MGP缺陷所导致的相关疾病治疗新方法。The matrix gamma-carboxyglutamate protein(MGP),a vitamin K-dependent protein,inhibits arterial calcification.The substance's ability to inhibit calcification is linked to its post-translational modifications,specificallyγ-glutamyl carboxylation and phosphorylation.The molecular mechanism of the calcification inhibitor remains unclear due to its low solubility and complicated post-translational modifications.In this section,we summarize current research and ongoing debates about post-translational modifications of MGP and its mechanism for inhibiting calcification.We reviewed recent research on diseases associated with MGP deficiency,such as cardiovascular disease,chronic kidney disease,and Keutel syndrome.Hopefully,this review can help us understand how MGP functions as a vascular calcification inhibitor and identify potential treatments for diseases resulting from its dysfunction.

关 键 词：基质γ-羧基谷氨酸蛋白 翻译后修饰 钙化抑制 

分 类 号：R543[医药卫生—心血管疾病] R692[医药卫生—内科学] R363[医药卫生—临床医学]