“…These include heparan sulfated proteoglycans (HSPGs), thrombomodulin (TM), and tissue factor pathway inhibitor (TFPI). [16][17][18] Endothelial cells produce HSPGs, a small amount of which is expressed on the luminal surface in contact with the flowing blood. The HSPGs are a binding site for antithrombin (AT), which then is fully capable of inactivating thrombin produced in the vicinity of the HSPG.…”
Section: Other Anticoagulant Properties Of Endothelial Cellsmentioning
confidence: 99%
“…Therefore, any thrombin circulating in large vessels will be quickly extracted when the blood passes through a capillary. 16 TFPI on the endothelial cell surface prevents additional thrombin generation by acting as an upstream inhibitor of FXa and FVIIa. It irreversibly binds to FXa, then forms a quaternary complex between TFPI, FXa, FVIIa, and TF, preventing further participation of these protein molecules in the generation of additional thrombin.…”
Section: Other Anticoagulant Properties Of Endothelial Cellsmentioning
Objective -To review the current model describing coagulation processes, including the critical contributions of cells. Data Sources -Original research articles, scientific reviews, and textbooks. Data Synthesis -Normal hemostasis is vital for prevention of blood loss, but controls are necessary to limit coagulation to the site of injury. The previous cascade model of blood coagulation, although refined and updated over the last few decades, is flawed as a description of how hemostasis occurs in vivo. The recently proposed model incorporates the vital role of cells in coagulation processes, and corrects deficiencies of the older cascade models. Conclusions -The cell-based model of coagulation provides a description of coagulation that more likely reflects hemostatic processes as they occur in vivo.
“…These include heparan sulfated proteoglycans (HSPGs), thrombomodulin (TM), and tissue factor pathway inhibitor (TFPI). [16][17][18] Endothelial cells produce HSPGs, a small amount of which is expressed on the luminal surface in contact with the flowing blood. The HSPGs are a binding site for antithrombin (AT), which then is fully capable of inactivating thrombin produced in the vicinity of the HSPG.…”
Section: Other Anticoagulant Properties Of Endothelial Cellsmentioning
confidence: 99%
“…Therefore, any thrombin circulating in large vessels will be quickly extracted when the blood passes through a capillary. 16 TFPI on the endothelial cell surface prevents additional thrombin generation by acting as an upstream inhibitor of FXa and FVIIa. It irreversibly binds to FXa, then forms a quaternary complex between TFPI, FXa, FVIIa, and TF, preventing further participation of these protein molecules in the generation of additional thrombin.…”
Section: Other Anticoagulant Properties Of Endothelial Cellsmentioning
Objective -To review the current model describing coagulation processes, including the critical contributions of cells. Data Sources -Original research articles, scientific reviews, and textbooks. Data Synthesis -Normal hemostasis is vital for prevention of blood loss, but controls are necessary to limit coagulation to the site of injury. The previous cascade model of blood coagulation, although refined and updated over the last few decades, is flawed as a description of how hemostasis occurs in vivo. The recently proposed model incorporates the vital role of cells in coagulation processes, and corrects deficiencies of the older cascade models. Conclusions -The cell-based model of coagulation provides a description of coagulation that more likely reflects hemostatic processes as they occur in vivo.
“…21 In a hemostatic response, they produce key components of platelet activation and aggregation, including von Willebrand factor (vWf), fibronectin and thrombospondin, ultimately leading to the initiation of the coagulation cascade. 22 These dynamic thrombotic functions are important, as thrombus formation is a key element in atherosclerosis progression.…”
Section: Regulation Of the Coagulation Cascadementioning
Coronary artery disease (CAD) and erectile dysfunction (ED) are both highly prevalent conditions that frequently coexist. Additionally, they share mutual vascular risk factors, suggesting that they are both manifestations of systemic vascular disease. The role of endothelial dysfunction in CAD is well established. Normal erectile function is primarily a vascular event that relies heavily on endothelially derived, nitric oxide-induced vasodilation. Accordingly, endothelial dysfunction appears to be a common pathological etiology and mechanism of disease progression between CAD and ED. The risk factors of diabetes mellitus, hypertension, hyperlipidemia, obesity and tobacco abuse contribute to endothelial dysfunction. This article reviews the role of vascular endothelium in health, the abnormalities resulting from vascular risk factors, and clinical trials evaluating the role of endothelial dysfunction in ED.
“…a) Regulaci贸n de la hemostasia. El endotelio mediante diferentes mecanismos antiplaquetarios, anticoagulantes y fibrinol铆ticos, desempe帽a un papel fundamental en la regulaci贸n del balance hemost谩tico (22)(23)(24). 脡sto se debe a la secreci贸n regulada de agentes antiplaquetarios (s铆ntesis de adenosina, NO y prostaciclina), a la regulaci贸n de la coagulaci贸n que tiene como producto final la trombina (s铆ntesis del inhibidor del factor tisular, activaci贸n de la prote铆na C a trav茅s de la trombomodulina y activaci贸n de la antitrombina III) (25, 26) y a la secreci贸n de mol茅culas que activan la fibrin贸lisis (activador tisular de plasmin贸geno (tPA)) (27).…”
INTRODUCCI脫NLa c茅lulas endoteliales, entre otras funciones, regulan el tono y permeabilidad vascular, adhesi贸n leucocitaria y la hemostasia (1). Dentro de los mecanismos que regulan las funciones del endotelio, la producci贸n de 贸xido n铆trico (NO) es de central importancia. ABSTRACT The endothelium helps to maintain the normal structure and homeostasis of the vasculature. However, chronic exposure to cardiovascular (CV) risk factors causes endothelial dysfunction, a phenomenon that is characterized by inflammation, reduced bioavailability of nitric oxide (NO) and a prothrombotic state. Epidemiological studies have shown that regular consumption of fruits and vegetables reduces CV risk, which has caused interest in knowing the bioactive compounds and the mechanisms involved. Among the components that protect the endothelium are antioxidants (vitamin C, vitamin E and polyphenols) and polyunsaturated fatty acids. Vitamin C and E promote vasodilatation protecting NO by blocking the reactive oxygen species (ROS). Polyphenols improve endothelial function primarily by increasing levels of NO, and inhibition of angiogenesis and platelet activation. Diets rich in polyunsaturated fatty acids have shown beneficial effects by reducing the gene expression of cyclooxygenase-2 and the expression of cell adhesion molecules. This review mainly highlights the current understanding of endothelial dysfunction and the protective effect of endothelial cells by bioactive components of fruits and vegetables.
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