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Endothelial cells at disturbed flow sites refer to endothelial cells lining blood vessels that are exposed to non-laminar, oscillatory, or multidirectional hemodynamic forces typically found at arterial branches, curvatures, or sites of vascular injury. These mechanical conditions prompt a unique reprogramming of endothelial gene expression and function compared to cells exposed to stable, laminar flow[1][2][3][4]. In these regions, endothelial cells show increased inflammation, loss of vascular barrier integrity, upregulation of cell adhesion molecules, production of pro-inflammatory cytokines, and can undergo endothelial-to-mesenchymal and immune cell-like transitions[2][3][4][7]. These phenotypic changes drive the development and progression of atherosclerotic plaques and other vascular pathologies. The “target” is not a single molecular entity but a functional/phenotypic state of endothelial cells defined by their microenvironment rather than a single gene or protein product. Therapeutic strategies in this context are aimed at modulating the signaling pathways or gene expression programs within these cells, not targeting the cells directly with receptor or enzyme inhibitors[2][3][4][1].
drugs do not bind this entity; however, some drugs target pathways and responses in these cells
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