Figure 1.

Protease activated receptors (PARs), pulmonary artery smooth muscle cells (PASMCs), microparticles (MPs), and inflammation are associated with pulmonary thromboembolism (PTE). Biomedical research has shown that PARs modulate thrombosis by activating ECs, and functional proteins (e.g., CapG, transgelin, and ACE2) in PASMCs have an important function in pulmonary vasoconstriction. Clinical research links MPs and hypercoagulability to venous thromboembolism. Epidemiological studies have shown that inflammation is a risk factor for PTE.