The endothelium in atherogenesis

The focus of this article is an overview of the endothelial changes that in itiate and perpetuate the process of atherogenesis. The endothelium can und ergo a series of changes which allow it to participate in the inflammatory response; this is known as endothelial cell activation (ECA). The five core changes of ECA are loss of vascular integrity; expression of leucocyte adh esion molecules; change in phenotype from antithrombotic to prothrombotic; cytokine production, and upregulation of HLA molecules. The diverse effects of ECA share a common intracellular control mechanism through the activati on of the transcription factors including Nuclear Factor kappa B. ECA is an initiating step in atherogenesis. Modified low density lipoprotei ns are probably the major cause of endothelial cell activation in atherogen esis, and become especially so after oxidation, glycation (in diabetes) or incorporation in immune complexes. In antiphospholipid syndrome (APS), anti endothelial cell antibodies have been detected in up to 67% of patients. In vitro studies suggest that aPL causes ECA and thus lead to speculation tha t aPL by causing ECA may initiate atherogenesis. Further clinical and in vi tro studies are required to address these issues.