After mammalian peripheral nerve injury, axons can regenerate very long distance. In certain conditions, the central nervous system can also partially regenerate after damage. Nogo has been proved to be one of the myelin-associated inhibitors, after central nerve injury increased Nogo release, enhanced Nogo expression, start-up process of apoptosis, leading to neuronal death. In this paper, we summed up the mechanism of action of Nogo from Nogo-A, Nogo-66, soluble NgR fragments, RhoA enzyme and Rho-A/Rho kinase signaling pathway, calcium ion aspects, and discussed its application prospect in nerve regeneration after optic nerve injury.