Mechanisms of endothelial dysfunction during aging: Predisposition to thrombosis.

One of the risk factors for developing cardiovascular disease (CVD) is aging. In the elderly endothelial dysfunction occurs as altered endothelial ability to regulate hemostasis, vascular tone and cell permeability. In addition, there are changes in the expression and plasma levels of important endothelial components related to endothelial-mediated modulation in hemostasis. These include alterations in the metabolism of nitric oxide and prostanoides, endothelin-1, thrombomodulin and Von Willebrand factor. These alterations potentiate the pro-coagulant status developed with aging, highlighting the endothelial role in the development of thrombosis in aging.

Sepúlveda C ，Palomo I ，Fuentes E 《-》

Atorvastatin reduces the proadhesive and prothrombotic endothelial cell phenotype induced by cocaine and plasma from cocaine consumers in vitro.

Cocaine consumption is a risk factor for vascular ischemic complications. Although endothelial dysfunction and accelerated atherosclerosis have been observed in cocaine consumers, the mechanisms underlying their pathogenesis are not fully understood. This study aimed at identifying the effects of atorvastatin in relation to a proadhesive and prothrombotic phenotype induced by cocaine and plasma from chronic cocaine users on endothelial cells. Human umbilical vein endothelial cells were exposed to either cocaine or platelet-free plasma (PFP) from chronic cocaine consumers in the presence or absence of 10 μmol/L of atorvastatin. Atorvastatin significantly reduced the enhanced platelet adhesion that was induced by cocaine and PFP from chronic cocaine consumers, as well as the release of the von Willebrand factor. Atorvastatin also avoided striking alterations on cell monolayer structure triggered by both stimuli and enhanced NO reduction because of cocaine stimulation through disrupting interactions between endothelial nitric oxide synthase (eNOS) and caveolin-1, thus increasing eNOS bioavailability. Cocaine-increased tissue factor-dependent procoagulant activity and reactive oxygen species generation were not counteracted by atorvastatin. Although monocyte chemoattractant protein-1 levels were not significantly higher than controls either under cocaine or PFP stimulation, atorvastatin completely avoided monocyte chemoattractant protein-1 release in both conditions. Platelets stimulated with cocaine or PFP did not express P-selectin, glycoprotein IIb/IIIa, or CD40L and failed to adhere to resting human umbilical vein endothelial cell. Cocaine and patient plasma equally induced a proadhesive and prothrombotic phenotype in endothelial cells, except for von Willebrand Factor release, which was only induced by PFP from chronic cocaine consumers. Atorvastatin improved endothelial cell function by reducing cocaine-induced and PFP from chronic cocaine consumer-induced effects on platelet adhesion, cell architecture, and NO production.

Sáez CG ，Pereira-Flores K ，Ebensperger R ，Panes O ，Massardo T ，Hidalgo P ，Mezzano D ，Pereira J ... -  《-》

Progression of the prothrombotic state in aging Bmal1-deficient mice.

Hemmeryckx B ，Van Hove CE ，Fransen P ，Emmerechts J ，Kauskot A ，Bult H ，Lijnen HR ，Hoylaerts MF ... -  《-》

Homeostasis of Hemostasis: The Role of Endothelium.

Forming an interface with virtually every other organ, endothelium has a strategic role in modulating vascular homeostasis. While its miscellany of functions includes regulation of vasomotor tone, promotion, and prevention of vascular growth, and modulation of inflammatory and hemostatic processes, it functions critically in maintaining the balance of hemostasis in health. Whereas endothelium has been recognized to influence all stages of hemostasis, new evidence suggests it to have a primary role for thrombin generation. Endothelial dysfunction is being increasingly appreciated in several pathological states and particularly, by virtue of its critical role in hemostasis, in causing thrombosis in a multitude of diseases.

Kazmi RS ，Boyce S ，Lwaleed BA 《-》

[Features of metabolic activity of vascular endothelium in patients with pulmonary tuberculosis].

Kaminskaia GO ，Abdullaev RIu ，Komissarova OG 《-》