ACSL3 / GABARAPL2 Ameliorates Vascular Endothelial Cell Aging and Injury Through Protective Autophagy to Alleviate Ferroptosis

levels, and alleviated ferroptosis under oxidative stress. GABARAPL2 upregulated ACSL3 expression, which further promoted autophagy and inhibited ferroptosis. Autophagy inhibition reversed these protective effects, indicating that GABARAPL2/ACSL3-mediated autophagy plays a key role in mitigating ferroptosis and oxidative stress. GABARAPL2/ACSL3 improves VEC aging and injury by promoting protective autophagy and reducing ferroptosis, thereby improving cellular viability under oxidative stress. These findings offer a potential therapeutic target for diseases associated with endothelial dysfunction.