ArticleShock (Augusta, Ga.)2026
Plasma Proteomic Signatures of Coagulopathy Following Traumatic Injury: Links to Biomechanics and Patient Outcomes.
Article in Shock (Augusta, Ga.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Characterizing the impact of traumatic brain injury phenotype on coagulation dynamics in severely injured patients.Thrombosis research · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
backgroundTraumatic injury is a leading cause of death, in large part driven by coagulopathy-associated hemorrhage and thrombotic complications. Identification of biological pathways and therapeutic targets has been limited. We performed a proteomic analysis using plasma isolated from trauma patients and assessed the proteome relation to clot formation and stability.
methodsPlatelet-poor plasma was isolated from trauma patients upon emergency department arrival. Coagulation was characterized using rheology, turbidity, and confocal microscopy. Proteomics were measured using liquid chromatography-mass spectrometry and compared between: 1) healthy donors vs . trauma patients, 2) nonsevere vs . severe injury, 3) survived vs . deceased patients, 4) penetrating vs . blunt injuries, 5) traumatic brain injury (TBI) vs . no-TBI, and 6) presence vs . absence of physiological shock. Spearman correlations were calculated between coagulation tests, clinical vitals, and proteomics data. Gene ontology and Search Tool for the Retrieval of Interacting Genes/Proteins analysis identified enrichment of biological processes and interconnectedness of mortality-related proteins.
resultsHemostatic processes were enriched in healthy donors, severe injury patients, surviving patients, no-TBI patients, and patients not exhibiting shock. Plasminogen activator inhibitor 3 was in higher abundance in those who survived their injuries compared with those who died. Plasminogen activator inhibitor 3 was correlated with faster clotting time, thrombin generation, and decreased D-dimer. Proteins higher in deceased patients compared with those who survived, such as prostaglandin-H2 isomerase, related to immune activity, correlated with weaker clots and increased D-dimer.
conclusionsThis exploratory analysis of plasma proteomics in trauma patients identified potential markers related to coagulation and immune activity, which may contribute to coagulopathy-associated mortality after injury and serve as therapeutic targets.
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.