N-acetylcysteine amide alleviates pathological neovascularization through mitochondrial protection and energy metabolism reprogramming of vascular endothelial cells.

ABSTRACT: Hypoxia-induced pathological neovascularization is a major contributing factor to a variety of diseases across different age groups. Currently, the predominant therapeutic approach involves the repeated injection of anti-vascular endothelial growth factor (VEGF) agents, which are associated with several adverse effects that limit their long-term application. This study concentrates on the upstream regulators of VEGF within vascular endothelial cells (VECs) and uses the oxygen-induced retinopathy mouse model to demonstrate that N-acetylcysteine amide (NACA) exhibits significant antiangiogenic properties both in vitro and in vivo. Notably, NACA preserves mitochondrial homeostasis and mitigates mitochondrial reactive oxygen species (mtROS) in VECs. Moreover, smart RNA sequencing and the Oxyge

SUBMITTER: Lin J 

PROVIDER: S-EPMC12663691 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature