ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
GLS1-Mediated Redundancy in Glutamate Accelerates Arterial Calcification via Activating NMDAR/Ca
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Glutamine metabolism in health and disease.Signal transduction and targeted therapy · 2026Review
- Glutaminase 1 in Vascular Disease: Linking Metabolic Reprogramming to Atherosclerosis Progression and Stability.Journal of cardiovascular translational research · 2026Review
- The Glutamine-α-Ketoglutarate Metabolic Axis Controls Vascular Smooth Muscle Cell Function.Cells · 2026Article
- Automated assessment of breast arterial calcification: a new frontier in cardiovascular risk prediction.Frontiers in cardiovascular medicine · 2026Review
- UPLC-MS/MS-based metabolomics analysis identifies disease-associated metabolic signatures of B cells from patients with IgG4-RD.Frontiers in immunology · 2026Article
- Article
- Lactate-Activated GPR132-Src Signal Induces Macrophage Senescence and Aggravates Atherosclerosis Under Diabetes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- GLS1-Mediated Redundancy in Glutamate Accelerates Arterial Calcification via Activating NMDAR/CaAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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Authors and funding
19 authors.
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Abstract
Arterial calcification is a powerful predictor of both the events and mortality associated with cardiovascular diseases in chronic kidney disease (CKD) patients. GLS1 (glutaminase 1), a rate-limiting enzyme catalyzing the conversion of glutamine to glutamate, is disordered in various cardiovascular diseases. However, the potential interplay between GLS1-mediated glutamate production and arterial calcification remains poorly understood. Here, LC-MS/MS analysis of CKD patients' samples shows an abnormally elevated activity of GLS1, reflected by the increased glutamate/glutamine ratio. Moreover, GLS1 activity is positively correlated with arterial calcification progression, and its expression is upregulated in calcified arteries. Treatment with GLS1 inhibitors or knockdown of GLS1 alleviates osteogenic reprogramming. In contrast, glutamate administration boosts the development of arterial calcification. Mechanistically, GLS1 redundancy-regulated glutamate superfluity stimulates the activation of N-methyl-d-aspartate receptors (NMDAR), leading to Ca
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