Fibrin Dynamics in Hemostasis and Thrombosis

Fibrin plays a central role in the final stages of the coagulation cascade, transforming soluble fibrinogen into an insoluble network that stabilises the platelet plug and achieves haemostasis. The architecture and mechanical properties of this fibrin mesh govern clot stability, permeability and susceptibility to enzymatic degradation. In thrombosis, aberrant fibrin formation or impaired breakdown can lead to vessel occlusion and life-threatening events such as myocardial infarction, stroke and venous thromboembolism. Recent work has elucidated how factors including fibre diameter, cross-linking by activated factor XIII, post-translational modifications and hydrodynamic forces alter fibrin structure and resistance to fibrinolysis. Understanding these interrelated processes offers opportunities to refine diagnostics, predict clinical risk and develop targeted therapies that restore the balance between clot formation and dissolution.

Research from Nature Portfolio

Investigations into the presence of circulating fibrin-rich aggregates in patients with acute pulmonary embolism have confirmed that these microstructures persist both before and after clotting. High-resolution microscopy revealed that low-molecular-weight heparin markedly reduces their abundance, raising questions about their role in thrombus propagation or resolution. Complementary multiscale modelling studies have integrated molecular kinetics and three-dimensional clot architecture to simulate the progression of a lysis front. These models show that the interplay between tissue-type plasminogen activator concentration, plasmin generation and fibrin network density determines the speed and uniformity of clot dissolution, providing quantitative insights into the conditions required for effective thrombolysis.

Fibrin Dynamics in Hemostasis and Thrombosis publication trend

The graph below shows the total number of articles in fibrin dynamics in hemostasis and thrombosis across all publications each year (not limited to Nature Index journals).

Technical terms

Fibrinogen: A soluble plasma glycoprotein that is converted to fibrin by thrombin.

Fibrin: The insoluble polymer formed by fibrinogen cleavage, creating the scaffold of a blood clot.

Haemostasis: The physiological process that stops bleeding by forming a stable clot at sites of vascular injury.

Thrombosis: Pathological clot formation within blood vessels, leading to partial or complete obstruction.

Fibrinolysis: The enzymatic breakdown of fibrin by plasmin, restoring vessel patency after clot formation.

Thrombus: A consolidated mass of platelets, fibrin and trapped blood cells within the vasculature.

References

1. Fibrin clot properties in cardiovascular disease: from basic mechanisms to clinical practice. Cardiovascular Research (2023).
2. Tissue‐type plasminogen activator (tPA) homozygous Tyr471His mutation associates with thromboembolic disease. MedComm (2023).
3. Post-translational modifications of fibrinogen: implications for clotting, fibrin structure and degradation. Molecular Biomedicine (2024).
4. Plasma from patients with pulmonary embolism show aggregates that reduce after anticoagulation. Communications Medicine (2023).
5. Fibrin Fiber Stiffness Is Strongly Affected by Fiber Diameter, but Not by Fibrinogen Glycation. Biophysical Journal (2016).
6. Hindered dissolution of fibrin formed under mechanical stress. Journal of Thrombosis and Haemostasis (2011).
7. Molecular and Physical Mechanisms of Fibrinolysis and Thrombolysis from Mathematical Modeling and Experiments. Scientific Reports (2017).