Regulation of macrophage fibrinolysis during venous thrombus resolution.

ABSTRACT:

Background

Venous thromboembolism (VTE), which includes pulmonary embolism (PE) and deep vein thrombosis (DVT), is a serious cardiovascular disease with significant mortality and morbidity. Clinically, patients with faster resolution of a venous thrombi have improved prognosis. Urokinase-plasminogen activator (uPA), produced by macrophages, is a key mediator of fibrinolysis required for resolving venous thrombi and restoring vascular integrity. The major macrophage protein, plasminogen activator inhibitor type-2 (PAI-2), was originally identified as an inhibitor of uPA and is implicated in the modulation of pathways affecting fibrinolytic uPA activity, however its direct role in blocking uPA-mediated clot lysis is not known.

Objective

To determine the contribution of macroph

SUBMITTER: Johnson TA 

PROVIDER: S-EPMC11486561 | biostudies-literature | 2024 Nov

REPOSITORIES: biostudies-literature