ArticleAnnals of surgery2025
Endothelial Cell Calcium Influx Mediates Trauma-induced Endothelial Permeability.
Article in Annals of surgery, 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
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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.
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Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- Shock Induced Endotheliopathy and High Trauma Mortality-Fight-or-Flight Response Revisited.International journal of molecular sciences · 2026Review
- Plasma Constituents Promote Endothelial Thromboinflammatory Dysfunction After Hemorrhagic Shock.Shock (Augusta, Ga.) · 2026Article
- Trauma-Induced Coagulopathy: A Review of Specific Molecular Mechanisms.Diagnostics (Basel, Switzerland) · 2025Review
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveTo investigate whether ex vivo plasma from injured patients causes endothelial calcium (Ca 2+ ) influx as a mechanism of trauma-induced endothelial permeability.
backgroundEndothelial permeability after trauma contributes to postinjury organ dysfunction. While the mechanisms remain unclear, emerging evidence suggests intracellular Ca 2+ signaling may play a role.
methodsEx vivo plasma from injured patients with "low injury/low shock" (injury severity score <15, base excess ≥-6 mEq/L) and "high injury/high shock" (injury severity score ≥15, base excess <-6 mEq/L) were used to treat endothelial cells. Experimental conditions included Ca 2+ removal from the extracellular buffer, cyclopiazonic acid pretreatment to deplete intracellular Ca 2+ stores, and GSK2193874 pretreatment to block the transient receptor potential vanilloid 4 (TRPV4) Ca 2+ channel. Live cell fluorescence microscopy and electrical cell-substrate impedance sensing were used to assess cytosolic Ca 2+ increases and permeability, respectively. Western blot and live cell actin staining were used to assess myosin light chain phosphorylation and actomyosin contraction.
resultsCompared with low injury/low shock plasma, high injury/high shock induced greater cytosolic Ca 2+ increase. Cytosolic Ca 2+ increase, myosin light chain phosphorylation, and actin cytoskeletal contraction were lower without extracellular Ca 2+ present. High injury/high shock plasma did not induce endothelial permeability without extracellular Ca 2+ present. TRPV4 inhibition lowered trauma plasma-induced endothelial Ca 2+ influx and permeability.
conclusionsThis study illuminates a novel mechanism of postinjury endotheliopathy involving Ca 2+ influx through the TRPV4 channel. TRPV4 inhibition mitigates trauma-induced endothelial permeability. Moreover, widespread endothelial Ca 2+ influx may contribute to trauma-induced hypocalcemia. This study provides the mechanistic basis for the development of Ca 2+ -targeted therapies and interventions in the care of severely injured patients.
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Registered trials
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