Akt, or protein kinase B, is an important signaling molecule that modulates many cellular processes such as cell growth, survival, and metabolism. However, the in vivo roles and effectors of Akt in retinal angiogenesis are not explicitly clear. We therefore investigated the effects of recombinant Akt on inhibiting vessels loss and on suppressing experimental retinal neovascularization in this model. We showed that, compared with control groups, administration of the recombinant Akt in the first phase of retinopathy markedly reduced capillary-free areas, and significantly decreased retinal neovascularization. These results indicate that Akt plays a critical role in the pathological process (vessels loss and neovascularization) of oxygen-induced retinopathy in a mouse model, which may provide a valuable therapeutic tool for ischemic-induced retinal diseases.