Molecular and cellular concepts in atherosclerosis.

摘要: Abstract Atherosclerosis is a complex disease of uncertain cause. Its pathobiology believed to represent an abnormal expression the processes vascular healing. Etiologic models derive from ‘response injury’ paradigm and can be divided into three separate stages: endothelial dysfunction, smooth muscle proliferation architectural disruption. The initiating event dysfunction unknown, but related low-density lipoproteins and/or their oxidized derivatives. Endothelial injury signalled cells media by routes: direct cell-cell interaction, secretion soluble growth factors monocyte-derived cytokines. Monocytes are recruited endothelium invade subintimal space interaction variety adhesion proteins receptors on both cell types. Smooth initiated change in phenotype ‘contractile’ ‘synthetic’ resulting binding fibronectin specific integrin receptors. Three functionally distinct activities may subtypes ‘synthetic phenotype’: migration intima, increased inappropriate extracellular matrix synthesis. loss normal regulatory control anchorage independence suggest relationship oncogenic transformation. Both result platelet-derived factor-like receptors, which initiates cascade intracellular molecular events leading either cytoskeletal locomotory restructuring or cycle activation. pathways also appear coregulated depend upon phosphorylation membrane, cytosolic nuclear proteins. Clinical atherosclerosis follow sudden integrity intimal plaque different mechanisms: fissuring, intraluminal rupture intramural hemorrhage vessel wall stress biochemistry.