MGP

更新于：2025-05-07

基本信息

别名

Cell growth-inhibiting gene 36 protein、matrix Gla protein、MGLAP

+ [1]

简介

Associates with the organic matrix of bone and cartilage. Thought to act as an inhibitor of bone formation.

关联

项与 MGP 相关的药物

CN118206648

专利挖掘

靶点

MGP

作用机制-

在研机构

北京赛斯维德生物科技有限公司

原研机构

北京赛斯维德生物科技有限公司

在研适应症

男性泌尿生殖系统疾病 [+3]

非在研适应症-

最高研发阶段药物发现

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 MGP 相关的临床结果

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100 项与 MGP 相关的转化医学

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0 项与 MGP 相关的专利（医药）

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1,272

项与 MGP 相关的文献（医药）

2025-05-01·Acta Physiologica

Vitamin K preserves gamma‐glutamyl carboxylase activity against carbamylations in uremia: Implications for vascular calcification and adjunct therapies

Article

作者: Gombert, Alexander ; Kramann, Rafael ; Grommes, Jochen ; Floege, Jürgen ; Kaushik, Suresh ; de la Puente‐Secades, Sofia ; Jankowski, Vera ; Ziegler, Susanne ; Kaesler, Nadine ; Kuppe, Christoph ; Roma, Leticia Prates ; Frisch, Janina ; Jankowski, Joachim

AbstractAimVascular calcification contributes to morbidity and mortality in aging and is accelerated in diabetes and in chronic kidney disease. Matrix Gla Protein is a potent inhibitor of vascular calcification, which is activated by the vitamin K‐dependent gamma‐glutamyl carboxylase (GGCX). However, through a currently unidentified mechanism, the activity of GGCX is reduced in experimental uremia, thereby contributing to the promotion of vascular calcifications. In this study, we aim to identify the cause of these functional alterations and to stimulate the enzyme activity by potential GGCX binding compounds as a new avenue of therapy.MethodsTwo rodent models of experimental uremia and human carotid plaques were assessed for GGCX activity and modifications, as well as calcification. In silico compound screening via BindScope identified potential binding partners of GGCX which were further validated in functional assays for enzymatic activity changes and for in vitro calcification. Mass spectrometry was applied to monitor molecular mass changes of the GGCX.ResultsMass spectrometry analysis revealed post‐translational modifications of the GGCX in uremic rats and mice, as well as in calcified human carotid plaques. Functional assays showed that the post‐translational carbamylation of GGCX reduced the enzyme activity, which was prevented by vitamin K2. Chrysin, identified by compound screening, stimulated GGCX activity, reduced calcium deposition in VSMCs, and oxidized GGCX at lysine 517.ConclusionIn conclusion, this study clearly demonstrates that the vitamin K‐dependent enzyme GGCX plays a significant role in uremic calcification and may be modulated to help prevent pathological changes.

2025-05-01·Clinica Chimica Acta

Vascular calcification inhibitors in chronic kidney disease

Review

作者: Viigimaa, Margus ; Leis, Liisi ; Adoberg, Annika ; Fridolin, Ivo ; Holmar, Jana ; Uhlin, Fredrik ; Luman, Merike

BACKGROUNDIncreased cardiovascular mortality due to multifactorial progressive arterial stiffness in chronic kidney disease is influenced by the disturbed balance between inducers and inhibitors of vascular calcification. The potential to enhance the protective effects of vascular calcification inhibitors through effective therapy could stimulate further research and collaboration. This systematic review aims to give a grounded overview of vascular calcification inhibitors and their serum levels in different stages of chronic kidney disease to demonstrate the dynamics during stages of declining kidney function and renal replacement therapy.METHODSThe systematic review was registered in the PROSPERO database on August 30th, 2023 (CRD42023459169). and conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyzes (PRISMA).RESULTSWe screened 463 articles, of which 192 were eligible, and investigated vascular calcification inhibitors or included values of their serum levels. Serum levels of fetuin-A, vitamin D, FGF-23, Klotho, osteopontin, matrix GLA protein, osteoprotegerin, magnesium, and sclerostin are demonstrated in tables and sparingly studied substances with a perspective towards better treatment options are found in Supplementary Table.CONCLUSIONEndogenous vascular calcification inhibitors could serve the role of valuable biomarkers to detect the process earlier and estimate the effect of treatment. The serum levels presented demonstrate the dynamics in different stages in chronic kidney disease and propose practical feedback for personalized treatment strategies. Manifold possible vascular calcification inhibitors under research set a promising starting point for more effective therapeutic interventions.

2025-04-01·Molecular Therapy

Dysregulation of astrocyte-derived matrix gla protein impairs dendritic spine development in pyridoxine-dependent epilepsy

Article

作者: Liang, Ziqi ; Guo, Weixiang ; Wu, Junjie ; Wang, Min ; Guo, Ye ; Liu, Qiang ; Qin, Dezhe

In spite of adequate seizure control, approximately 75% of pyridoxine-dependent epilepsy (PDE) patients with ALDH7A1 mutation still suffer from intellectual disability. However, the mechanisms underlying brain dysfunction in PDE patients are still unknown even when seizure control is achieved. In this study, we show that mice with specific deletion of Aldh7a1 from astrocytes, but not neurons, exhibit PDE, and have defective dendritic spine development and cognitive impairment when seizure occurrence is well controlled. Mechanistically, ALDH7A1 deficiency leads to dysregulation of astrocyte-derived matrix gla protein (MGP), one of the vitamin K-dependent proteins, thereby impairing dendritic spine development and synaptic transmission. Notably, supplementation of menaquinone-7, a form of vitamin K, promotes MGP activation and rescues defective dendritic spine development, abnormal synaptic transmission, and cognitive impairment in Aldh7a1-deficient mice. Therefore, our findings not only unravel the important role of ALDH7A1 in astrocytes contributing to the pathogenesis of PDE, but also provide a potential therapeutic intervention to ameliorate cognitive impairment in PDE beyond pyridoxine treatment.

项与 MGP 相关的新闻（医药）

2023-01-17

·生物谷

阳了个阳可导致骨质流失，“阳康”后也要注意合理补钙

最近一段时间，新冠病毒来势汹汹，不少人已经感受过了来自它的“攻击”，发烧、咽痛、咳嗽、肌肉酸疼、浑身无力、味觉嗅觉丧失……而研究发现：新冠感染还会引最近一段时间，新冠病毒来势汹汹，不少人已经感受过了来自它的“攻击”，发烧、咽痛、咳嗽、肌肉酸疼、浑身无力、味觉嗅觉丧失……而研究发现：新冠感染还会引起骨吸收细胞的炎症激活，从而在感染期和康复期导致严重的骨质流失，新冠肺炎患者的维生素K2(MK-7)水平也会显著降低。（奥地利和德国科学家Mangge等在《抗氧化剂》(antioxidants)杂志上发表“新冠肺炎患者维生素K2(MK-7)水平显著降低”）骨质流失会招来骨质疏松症这个“沉默的杀手”，从而增加骨折的危险性。生活中可能有人认为，骨质疏松症是老年人的专利，距离还很遥远，因此并不是很重视。实际上，骨质疏松症已经越来越年轻化，而且由于儿童和青少年时期是骨骼成长的重要阶段，大约有50%的骨量是在青春期累积的，当骨量积累到一定峰值之后就会慢慢进入减少期。因此，阳康后，不论是老人、中年人还是青少年以及儿童都应注意预防骨质流失。想要预防骨质疏松，先要打好营养基础，日常生活中要注意合理膳食。多吃富含钙的食物，如牛奶、奶酪、豆制品、鱼虾贝类，绿叶蔬菜、芝麻酱等。同时还要多摄入维生素A、C、D、K，这些都会影响骨量维持，其中维生素K至关重要。事实上，我们的骨骼和牙齿主要是由钙构成，它对保持骨骼的强壮和健康至关重要。当人体缺钙的时候，骨骼就像溶洞一样千疮百孔，就容易引起骨质疏松，“补钙”也就成为防治骨质疏松的必要手段，维生素K2则是补钙入骨的关键。维生素K2是一种脂溶性维生素，能够激活基质谷氨酸蛋白（MGP）和骨钙素蛋白（OC），从而将血液中钙离子精准输送至骨骼，形成“骨钙”，实现“促钙成骨”①。但维生素K2的来源相对较少，仅来源于动物内脏、蛋黄、动物油脂、发酵食物，有时候并不能满足身体所需。因此在选择钙制剂时，可选择含有维生素D以及维生素K2的产品。其中4-17岁的儿童、青少年建议选择妈咪爱钙维KD咀嚼片，其含有碳酸钙、维生素K2和维生素D3，三效合一，使钙真正补进骨骼中。在品质方面，妈咪爱钙维KD咀嚼片源自韩国领先药企韩美集团，并且还是蓝帽子保健食品（食健G202134000086），功效、安全均有保障。除了以上方法，也要避免食盐摄入过量、吸烟、酗酒等不良生活习惯，加强体育锻炼，保证充足的睡眠，多管齐下，才能更好的防治骨质疏松、骨量流失。参考资料 ①陈淑玲,赵瑾珠,郝燕.维生素K与儿童骨健康的研究进展[J].中国儿童保健杂志,2021,29(07):742-745. 陈杰鹏《维生素K2（MK-7）——科学、产业生态和未来》演讲。