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The extracellular region contains FVII/VIIa binding domains. Circulating (blood-borne) TF is mainly derived from its expression in blood cells (e.g., monocytes, macrophages, granulocytes, and platelets), platelet-free microparticles containing TF shed from cells, or even soluble TF protein the serum level can be easily measured by TF antigen, ELISA, TF procoagulant activity (PCA), and so forth (for review, see ).įull-length TF (Figure 1), a membrane integral glycoprotein (46 kDa), is a 263-amino acid single-chain polypeptide classified as CD142 (Type II cytokine receptor) with a 219-amino-acid extracellular N-terminus and a 23-amino-acid transmembrane domain followed by an intracellular 21-amino-acid C-terminus. The low expression is detected in the spleen, thymus, and liver. High TF expression is found in highly vascularized organs (cells) such as the brain (e.g., astrocytes), placenta (e.g., trophoblasts), and the lungs (e.g., alveolar cells) followed by the heart (e.g., cardiac myocytes, pericytes, fibroblasts), kidney, intestine, testes, and uterus (e.g., epithelial cells surrounding the organs). Tissue factor (TF), also known as factor III, essentially provides additional protection to vital organs prone to mechanical injury its strategic location is considered as a hemostatic envelope for arresting bleeding from vascular beds. Accordingly, TF suppression, anticoagulation, PAR blockade, or general anti-inflammation offers an array of therapeutical benefits for easing diverse pathological conditions. Apparently, TF hypercoagulability refuels a coagulation-inflammation-thrombosis circuit in “autocrine” or “paracrine” fashions, which triggers a wide spectrum of pathophysiology. TF diverse biological roles are associated with either coagulation-dependent or noncoagulation-mediated actions. Biochemically, extracellular TF signaling interfaced through protease-activated receptors (PARs) elicits cellular activation and inflammatory responses. This paper broadly covers seminal observations to discuss TF pathogenic roles in relation to diverse disease development or manifestation. TF overexpression/hypercoagulability often observed in many clinical conditions certainly expands its role in proinflammation, diabetes, obesity, cardiovascular diseases, angiogenesis, tumor metastasis, wound repairs, embryonic development, cell adhesion/migration, innate immunity, infection, pregnancy loss, and many others. TF classical role in initiating the extrinsic blood coagulation and its direct thrombotic action in close relation to cardiovascular risks have long been established.
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Emerging evidence shows a broad spectrum of biological functions of tissue factor (TF).