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Diagram showing the location of endothelial cells

The endothelium is the thin layer of cells that line the interior surface of blood vessels,[1] forming an interface between circulating blood in the lumen and the rest of the vessel wall. Endothelial cells line the entire circulatory system, from the heart to the smallest capillary. These cells reduce turbulence of the flow of blood allowing the fluid to be pumped farther.

Endothelial tissue is a specialized type of epithelium tissue (one of the four types of biological tissue in animals). More specifically, it is simple squamous epithelium.

The endothelium normally provides a non-thrombogenic surface because it contains heparan sulphate which acts as a cofactor for activating antithrombin III, a protease that cleaves several factors in the coagulation cascade.



The foundational model of anatomy makes a distinction between endothelial cells and epithelial cells on the basis of which tissues they develop from and states that the presence of vimentin rather than keratin filaments separate these from epithelial cells.[2]

Endothelium of the interior surfaces of the heart chambers are called endocardium. Both blood and lymphatic capillaries are composed of a single layer of endothelial cells called a monolayer.


Endothelial cells are involved in many aspects of vascular biology, including:

In some organs, there are highly differentiated endothelial cells to perform specialized 'filtering' functions. Examples of such unique endothelial structures include the renal glomerulus and the blood-brain barrier.


Endothelial dysfunction, or the loss of proper endothelial function, is a hallmark for vascular diseases, and is often regarded as a key early event in the development of atherosclerosis. Impaired endothelial function is often seen in patients with coronary artery disease, diabetes mellitus, hypertension, hypercholesterolemia, as well as in smokers. Endothelial dysfunction has also been shown to be predictive of future adverse cardiovascular events. One of the main mechanisms of endothelial dysfunction is the diminishing of nitric oxide, often due to high levels of asymmetric dimethylarginine, which interfere with the normal L-arginine-stimulated nitric oxide synthesis. The most prevailing mechanism of endothelial dysfunction is an increase in reactive oxygen species, which can impair nitric oxide production and activity via several mechanisms.[3] The signalling protein ERK5 is essential for maintaining normal endothelial cell function [4].

See also




  1. ^ endothelium at Dorland's Medical Dictionary
  2. ^ "FMA". Retrieved 2008-12-12.  
  3. ^ Deanfield J, Donald A, Ferri C, Giannattasio C, Halcox J, Halligan S, Lerman A, Mancia G, Oliver JJ, Pessina AC, Rizzoni D, Rossi GP, Salvetti A, Schiffrin EL, Taddei S, Webb DJ (January 2005). "Endothelial function and dysfunction. Part I: Methodological issues for assessment in the different vascular beds: a statement by the Working Group on Endothelin and Endothelial Factors of the European Society of Hypertension". J Hypertens 23 (1): 7-17. PMID 15643116.  
  4. ^ Roberts OL, Holmes K, Müller J, Cross DA, Cross MJ. (Dec 2009). "ERK5 and the regulation of endothelial cell function.". Biochem Soc Trans. 37 (6): 1254-9. PMID 19909257.  


  • Molecular Biology of the CELL, 4th edition, Alberts et al., 2002

External links


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