AbstractPurpose of review
In spite of significant morbidity and mortality associated with venous thromboembolism, the underlying pathogenesis remains poorly understood.Recent findings
Clues to operant pathogenic mechanisms are found in the unique morphology and composition of these thrombi, which have substantial red blood cell and fibrin content. Recent studies have revealed biochemical and biophysical mechanisms that dictate fibrin structure in venous thrombi and promote retention of red blood cells within the contracted clots. These mechanisms include newly recognized contributions of fibrin network structure and factor XIII(a)-mediated fibrin crosslinking to venous thrombus composition, size, and stability.Summary
Continued work to elucidate mechanisms by which fibrin(ogen), factor XIII, and red blood cells contribute to venous thrombus formation, structure, and stability may expose novel molecular targets and strategies for reducing thrombosis and thrombotic complications in certain at-risk patients.