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Endothelial dysfunction may be involved in the development of atherosclerosis [5] [6] [7] and may predate vascular pathology. [ 5 ] [ 8 ] Endothelial dysfunction may also lead to increased adherence of monocytes and macrophages , as well as promoting infiltration of low-density lipoprotein (LDL) in the vessel wall. [ 9 ]
The lesions formed in the intima, and persistent inflammation lead to desquamation of endothelium, which disrupts the endothelial barrier, leading to injury and consequent dysfunction. [25] In contrast, inflammatory stimuli also activate NF-κB-induced expression of the deubiquitinase A20 ( TNFAIP3 ), which has been shown to intrinsically ...
The blood–brain barrier (BBB) is a highly selective semipermeable border of endothelial cells that regulates the transfer of solutes and chemicals between the circulatory system and the central nervous system, thus protecting the brain from harmful or unwanted substances in the blood. [1]
Endothelial activation is a proinflammatory and procoagulant state of the endothelial cells lining the lumen of blood vessels. [1] It is most characterized by an increase in interactions with white blood cells (leukocytes), and it is associated with the early states of atherosclerosis and sepsis , among others. [ 2 ]
Activated protein C also provides much protection of endothelial barrier function. Endothelial barrier breakdown, and the corresponding increase in endothelial permeability, are associated with swelling, hypotension and inflammation, all problems of sepsis. APC protects endothelial barrier function by inducing PAR-1 dependent sphingosine kinase ...
Endothelial cells form the wall of the BBB, while mural cells exist on the outer surface of this layer of endothelial cells. The mural cells also have their own abluminal layer which hosts pericytes that work to maintain the permeability of the barrier, and the epithelial cells filter the amount of toxins entering.
Circulating endothelial cells (CECs) are endothelial cells that have been shed from the lining of the vascular wall into the blood stream. [1] Endothelial cells normally line blood vessels to maintain vascular integrity and permeability, but when these cells enter into the circulation, this could be a reflection of vascular dysfunction and damage. [2]
This endothelial dysfunction leads to impaired myocardial blood flow reserve as evidence by echocardiography. [10] About 50% of diabetics with diabetic cardiomyopathy show pathologic evidence for microangiopathy such as sub-endothelial and endothelial fibrosis, compared to only 21% of non-diabetic heart failure patients. [11]