Key result
Elimination of fibrin γ-chain cross-linking in FGG3X mice resulted in a 1.5-fold increase in pulmonary emboli count compared to wild-type mice, demonstrating its essential role in clot stability.
Why the study?
Anticoagulation for venous thromboembolism is suboptimal for preventing embolic events, prompting investigation into clot structural and mechanical properties and how they influence in vivo embolism.
Does the elimination of fibrin γ-chain cross-linking by FXIIIa increase pulmonary embolism arising from inferior vena cava thrombi in mice?
Population
Murine model lacking activated Factor XIII fibrin γ-chain cross-linking (FGG3X)
Comparison
Elimination of fibrin γ-chain cross-linking (FGG3X) vs normal phenotype
Design
Preclinical animal study
Authors
Loading...
Supports fibrin cross-linking for clot stability in mice; leaves open whether FXIIIa targeting affects human thromboembolism risk.
Does the elimination of fibrin γ-chain cross-linking by FXIIIa increase pulmonary embolism arising from inferior vena cava thrombi in mice?
Effect estimate: 1.5-fold increase
p-value: p=<0.001
Elimination of fibrin γ-chain cross-linking reduces clot stability and increases pulmonary embolism in a murine model, highlighting its critical role in preventing thromboembolism.
Duval et al. (2021) studied Venous thromboembolism and pulmonary embolism. FGG3X mutation (elimination of fibrin γ-chain cross-linking) vs. Wild-type mice was evaluated on Pulmonary emboli count (1.5-fold increase, p=<0.001). Elimination of fibrin γ-chain cross-linking in FGG3X mice resulted in a 1.5-fold increase in pulmonary emboli count compared to wild-type mice, demonstrating its essential role in clot stability.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: