Role of inflammation in venous thrombosis formation and resolution

Venous thromboembolism (VTE) is a frequent disease associated with high mortality in case of pulmonary embolism and long-term complications that dramatically affect patient quality of life. Anticoagulants are the cornerstone of treatment and should be administered once VTE has been diagnosed to prevent early fatal and nonfatal recurrences. However, despite therapeutic advances, the long-term prognosis of VTE remains poor and is associated with increased bleeding risk due to the anticoagulant treatment. Studies have established that VTE is associated with the generation of a wide range of damage-associated molecular patterns, cytokines, and chemokines, promoting the recruitment of immune cells. This review summarized how these cells contribute to thrombus formation and resolution. We also discussed how the different cell types involved in VTE might interact with each other in these disease settings. We highlighted a major role of monocyte phenotypes in the different phases of VTE and how manipulating these cells might represent an interesting therapeutic strategy in addition to the anticoagulants. Finally, we discussed the critical implications these mechanisms might have in preventing or reducing the occurrence of long-term complications, including postthrombotic and postpulmonary embolism syndromes. Future directions should consider deciphering how inflammation is regulated in VTE to propose new therapeutic strategies to improve therapeutic management and patient outcomes.