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Uterine blood and oxygen supply refers to the vital physiological process of delivering oxygen and nutrients via the maternal cardiovascular system to the uterine tissues and the developing fetus [6, 13]. This process is highly regulated by complex molecular pathways, including the nitric oxide (NO) system, vascular endothelial growth factor (VEGF) signaling, and steroid hormones such as estrogen and progesterone, which collectively manage vascular resistance and remodeling [3, 9, 14]. During pregnancy, the uterine vasculature undergoes profound adaptations, such as spiral artery remodeling, to ensure a high-volume, low-resistance supply essential for fetal growth [7, 14]. Dysregulation of this supply is a primary driver of pregnancy-related complications like preeclampsia, fetal growth restriction (FGR), and placental insufficiency [7, 15]. Therapeutic strategies aimed at enhancing this supply typically target downstream effectors, such as using PDE5 inhibitors like sildenafil to promote vasodilation or targeting the VEGF pathway to enhance angiogenesis and uterine perfusion [2, 5, 15].
Promotion of uterine vascular relaxation and remodeling through phosphodiesterase-5 (PDE5) inhibition, nitric oxide (NO) donation, calcium channel blockade, and activation of the VEGF-angiogenesis pathway.
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