Shock (Augusta, Ga.) · 2026
Plasma Proteomic Signatures of Coagulopathy Following Traumatic Injury: Links to Biomechanics and Patient Outcomes.
СтатьяНазвание и аннотация: Перевод в очереди
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Gosselin Andrew R, Parker Olivia, Ali Sinan Hajer, Hanna Joseph S, Goswami Julie, Tutwiler Valerie
Аннотация
BACKGROUND: Traumatic 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.
METHODS: Platelet-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.
RESULTS: Hemostatic 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.
CONCLUSIONS: This 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.
METHODS: Platelet-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.
RESULTS: Hemostatic 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.
CONCLUSIONS: This 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.