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Endothelial cell differentiation refers to the process by which mesodermal progenitors or angioblasts transition into specialized endothelial cells (ECs), which are crucial for forming new blood and lymphatic vessels during embryonic development and tissue repair[1][2][3][4][5]. This process is orchestrated by tightly regulated signaling pathways—such as Hedgehog, WNT, BMP, VEGF, Notch, and FGF—and a network of transcription factors like those from the ETS family (especially Etv2/ER71), which together direct cell fate and ensure proper vascular patterning and organ-specific endothelial heterogeneity[1][2][3][5][7][8]. Disruption of endothelial cell differentiation can result in lethal defects in vascular development, as well as pathologies such as abnormal angiogenesis in tumors, cardiovascular disease, and failure of tissue regeneration[4][7]. Key clarifications: - Endothelial cell differentiation is not a "target" in the sense required for structured drug/therapeutic databases (e.g., is not a receptor such as "Vascular endothelial growth factor receptor 2"). - The actual pharmacological targets are upstream molecules and pathways that regulate this process (e.g., VEGF-A, VEGFR2, FGF2, BMP4, Notch signaling components)[2][3][5][6].
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