The axon is a unique feature of the neurons, and its length can reach hundreds and sometimes thousands times of the diameter of the cell body. To maintain normal functions, a large amount of materials need to be transported from the soma to the axon terminals or from the axon terminals to the soma. Damage of axon transport leads to disruption of neuronal functions and eventually results in cell death. Impairment of axon transport is among the earliest symptoms of some optic neuropathies, and is therefore likely the potential target of intervention. In the animal models of glaucoma and retinal ischemia, decline in axon transport is one of the earliest signs. Leber's hereditary optic neuropathy (LHON) and autosomal dominant optic atrophy (ADOA) are known diseases caused by mitochondrial dysfunction. Conceivably, long distance axon transport is especially sensitive to energy metabolism and is likely affected at certain degree in the LHON and ADOA, but has not been paid enough attention. In this review, we compared the pathogenesis, clinical symptoms and therapies of the above optic neuropathies, attempt to highlight the common aspects and to reveal the relationship among optic neuropathies, energy metabolism and axon transport in order to provide new clues for the therapy.