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The distinction between physiological angiogenesis and pathological angiogenesis matters enormously here
Chronic hyperglycemia-induced ROS overproduction, primarily derived from mitochondrial ETC leakage and NOX activation, leads to eNOS uncoupling due to BH4 oxidation, reducing NO bioavailability and impairing vasodilation (Giacco and Brownlee, 2010)
Without adequate levels, this conjugation process stalls, and hormone byproducts can recirculate instead of being cleared
Noncanonical E2 recruitment by the autophagy E1 revealed by Atg7-Atg3 and Atg7-Atg10 structures
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