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Endometrial microvascular endothelial cells (HEMECs) are specialized endothelial cells that line the microvessels of the uterine endometrium (Innoprot, 2024). These cells are unique for their ability to undergo rapid, cyclic angiogenesis and regression in response to ovarian steroids during the menstrual cycle (Sigma-Aldrich, 2024). HEMECs play a critical role in physiological processes such as endometrial regeneration and menstruation, but their dysregulation is central to the pathogenesis of several gynecological disorders, including endometriosis and endometrial cancer (NIH, 2024). In these conditions, HEMECs facilitate disease progression by supporting pathological angiogenesis and providing the necessary blood supply for lesion or tumor growth (Biorxiv, 2023). Consequently, these cells and their signaling pathways, particularly the VEGF/VEGFR axis, are significant targets for anti-angiogenic therapies (NIH, 2024). Drugs such as bevacizumab and various tyrosine kinase inhibitors, like lenvatinib, are used to disrupt the blood supply to diseased tissues by targeting these cells (NIH, 2024). While effective, these treatments can lead to systemic side effects like hypertension and impaired wound healing (NIH, 2024). Monitoring biomarkers such as CD31 and VEGFR2 is essential for evaluating the efficacy of therapies targeting the endometrial microvasculature (Sigma-Aldrich, 2024).
Anti-angiogenic agents inhibit the proliferation and migration of these cells by blocking growth factor signaling (e.g., VEGF), while hormonal therapies modulate their stability and permeability (Innoprot, 2024; NIH, 2024).
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