From Adipose Tissue Dysfunction to Venous Thromboembolism

Background/Objectives: Obesity is a major modifiable risk factor for venous thromboembolism (VTE), driven by adipose tissue dysfunction, chronic inflammation, endothelial dysfunction, hypercoagulability, impaired fibrinolysis, immunothrombosis, and venous stasis. Modern incretin-based therapies induce substantial weight loss and improve multiple cardiometabolic abnormalities that may influence thrombotic risk. To critically evaluate the biological rationale and clinical evidence supporting a potential role of incretin-based therapies in modifying VTE risk, while distinguishing mechanistic plausibility from proven clinical benefit and weight-loss-mediated effects from direct pharmacological actions.