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EN
The precise mechanisms of LDL oxidation in vivo are not well-known but the presence of several enzymes and agents capable of modifying LDL particles was noted in arterial wall. These reactive agents modify lipid, protein as well as antioxidant component of the LDL particles. Postsecretory modification in LDL structure trigger its atherogenic potential. LDL particles retained in the artery wall interact with the various forms of proteoglycans in the extracellular matrix, that increases the resident time of LDL in endothelial space and allows extensive modification. The modified forms of LDL are able to activate intimal cells and to trigger various inflammatory signals. In turn, activated intimal cells can secrete enzymes and agents capable of modifying LDL. These processes can initiate and maintain a vicious circle in the intima and lead to lesion progression.
EN
This paper reviews recent work regarding the molecules that mediate leukocyte-endothelial cell adhesion, describes the underlying principles of laukocyte migration, and discussed a model of the sequence of events that follows a leukocyte to attach to endothelium and migrate into tissue.Pathophysiological importance of the adhesion molecules in the development of different states of inflamation has been also presented.
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