Retinal injury is a common cause of profound and intractable loss of vision. Clinical outcomes are poor in both open and closed globe injuries because cell death, scarring, and a failure of tissue and axon regeneration are not ameliorated by current treatments. Much animal research is directed at understanding and modifying these pathologies, although results have yet to translate into clinical practice. Axotomy-induced retinal ganglion cell (RGC) death in mammals can be effectively reduced and axon regeneration enhanced over the short term. After retinal injury in mammals, the retinal pigment epithelium (RPE) and retinal glia either regenerate lost RPE and neuroretinal cells or form nonfunctional scars. An understanding of the mechanisms underlying injury responses is critical to the successful development of therapeutic strategies to promote ocular repair.
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