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Last update 08 May 2025

MGP

Last update 08 May 2025

Basic Info

Synonyms

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

+ [1]

Introduction

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

Drugs associated with MGP

CN118206648

Patent Mining

Target

MGP

Mechanism-

Active Org.

Bei Jing Sai Si Wei De Sheng Wu Ke Ji You Xian Gong Si

Originator Org.

Bei Jing Sai Si Wei De Sheng Wu Ke Ji You Xian Gong Si

Active Indication

Male Urogenital Diseases [+3]

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with MGP

100 Translational Medicine associated with MGP

0 Patents (Medical) associated with MGP

1,272

Literatures (Medical) associated with MGP

01 May 2025·Acta Physiologica

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

Article

Author: 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.

01 May 2025·Clinica Chimica Acta

Vascular calcification inhibitors in chronic kidney disease

Review

Author: 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.

01 Apr 2025·Molecular Therapy

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

Article

Author: 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.

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MGP

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