Relationship Between Neutrophil Extracellular Traps and Venous Thromboembolism: Pathophysiological and Therapeutic Role.

Venous thromboembolism (VTE), which includes pulmonary embolism (PE) and deep vein thrombosis (DVT), is a serious vascular disease that ranks third in cardiovascular-related deaths. Inflammation along with neutrophil extracellular traps (NETs) play a key role in the pathophysiology of VTE. This review focuses on articles that that evaluate the role of NETs in the development of VTE and their potential as therapeutic targets. Research has demonstrated that when NETs become overactivated, they take part in thrombotic activities, which is the opposite of their defensive functions under healthy conditions. When endothelial cells are activated, neutrophils are recruited very early, releasing NETs and initiating a thrombotic process. NETs promote thrombosis by directly activating factor XII (FXII), ultimately triggering platelet recruitment, and initiating the intrinsic coagulant pathway. Subsequently, monocytes and factors such as tissue factor join the process, further increasing NET formation, the inflammatory reactions and progression of venous thrombus. NETs play a crucial part in the intricate interaction between inflammation and thrombosis, where each triggers the other. High levels of NETs also correlate with the severity of VTE. These properties of NETs make them potential therapeutic targets for VTE prevention and treatment. This article aims to describe NETs, their occurrence, and how they relate to VTE. Taking into account what is now known, the function of NETs as targets for treatment in VTE using various approaches, the benefits and drawbacks of these approaches, and suggestions for the future are examined.