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Proliferating endothelial cells are the active cellular components of angiogenesis, the process by which new blood vessels grow from existing ones (Source: National Cancer Institute). In healthy adults, the endothelium is largely quiescent, but it becomes highly proliferative during wound healing, the menstrual cycle, and in various pathological states such as cancer and wet age-related macular degeneration (Source: PubMed, PMID: 12154373). These cells are characterized by the expression of specific markers like CD105 (Endoglin) and VEGFR2, which are often absent or expressed at low levels in stable vessels (Source: UniProt). Therapeutic targeting of these cells typically involves the use of monoclonal antibodies or small molecule inhibitors that block growth factor signaling, thereby inducing endothelial cell apoptosis or growth arrest to inhibit tumor vascularization (Source: FDA/Labeling for Bevacizumab). This approach aims to disrupt the nutrient and oxygen supply to diseased tissues while sparing the established, quiescent vasculature.
Drugs target these cells by inhibiting pro-angiogenic signaling pathways, primarily the VEGF/VEGFR axis, which prevents endothelial cell proliferation, migration, and survival (Source: NIH/NCI).
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