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.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
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
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
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
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.