Autophagy is a cellular process of degradation of damaged cytoplasmic components and regulates cell death and proliferation. Dysregulation of autophagy is involved in renal age-related diseases. However, its concise pathogenesis remains unclear. Ferroptosis is a new type of programmed cell death, accompanied by a large amount of iron accumulation and lipid peroxidation. Here, we investigated the cross-talk of autophagy with ferroptosis during renal aging. We generated conditional knockout mice in which Atg7 was genetically ablated specifically in endothelial cells (Atg7flox/flox;Tie2-Cre mice) and determined the ferroptosis pathway using these mice. In wild-type (WT) mice, autophagic flux was increased in aging kidneys compared with young kidneys. The accumulation of ferritin was abundantly increased in old-aged WT mice compared than young WT mice, which were colocalized with LC3. Genetic deletion of Atg7 specifically in endothelial cells resulted in decrease of autophagy induction during aging and led to a glomerulopathy with mesangial expansion, capillary wall dilatation, thickness of glomerular basement membrane, foot process effacement and glomerlosclerosis. The accumulation of ferritin was enhanced in old aged-Atg7flox/flox;Tie2-Cre mice that were accompanied by accumulation of reactive oxygen species and 4-hydroxynonenal and depletion of glutathione peroxidase 4 (GPX4). Pharmacologic inhibition of ferroptosis with liproxstatin reversed the endothelial cells-specific Atg7 deletion induced proteinuria and GPX4 expression in aging mice. Our data showed that autophagy in endothelial cells play a protective role in renal aging with suppressing ferroptosis and the regulation of endothelial autophagy and ferroptosis may be a therapeutic target to reduce the injury from renal aging.