ArticleThe Kaohsiung journal of medical sciences2025
Glutamate Exacerbates Traumatic Brain Injury-Induced Acute Lung Injury Through NMDAR/ROS/Ca
Article in The Kaohsiung journal of medical sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Dietary intakes of cysteine, glutamate, proline, and tryptophan are associated with hypertension risk in Chinese children and adolescents: a national cross-sectional study integrating machine learning.Frontiers in nutrition · 2026Article
- Glutamate Exacerbates Traumatic Brain Injury-Induced Acute Lung Injury Through NMDAR/ROS/CaThe Kaohsiung journal of medical sciences · 2025Article
- Circulating metabolome as key biomarkers for ventilator-associated pneumonia: Case-Control study in a tertiary care hospital of North India.International journal of critical illness and injury scienceArticle
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Authors and funding
3 authors.
Funding
Abstract
Traumatic brain injury (TBI) causes a high level of blood glutamate, which triggers host defense by activating oxidative stress and inflammation response. However, the concrete mechanism underlying its exacerbating effects on acute lung injury (ALI) severity remains unknown. In the present study, we aim to demonstrate the special role of N-methyl-D-aspartate receptor (NMDAR) in regulating glutamate-related inflammation signaling to facilitate the sustaining injury. After the interventions, blood glutamate concentration was measured using HPLC-MS/MS. The level of pro-inflammation cytokines, wet/dry weight ratio, protein concentration, and lung injury score were measured to examine the severity of lung damage. The oxidative status was evaluated by measuring the levels of reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD) activity, and intracellular Ca
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