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Great advances in retinal ganglion cells survival (RGCs), optic nerve preservation and regeneration have been made in the past 15 years. Nowadays, we know that RGCs are capable of regenerating the full length of the optic nerve, cross the chiasm, enter the brain and reinnervate visual targets. In order to obtain successful regeneration, RGCs need to activate signaling pathways related to cell survival and turn on their intrinsic growth capacity. Studies that aimed at blocking cell death and inhibiting apoptosis by B-cell lymphoma 2 (Bcl-2) overexpression showed an increase in cell survival, but these approaches were not sufficient to promote axon regeneration, even when axons were put in an permissive environment, as peripheral nerve graft (Inoue et al., 2002). Neither stimulating axon regeneration by intraocular inflammation, nor delaying axon degeneration by overexpression of Wlds protein, or inhibition of calpain activation (Figure 1C) (de Lima et al., 2016) showed any increase in cell survival. Nevertheless, Park et al. (2008) showed that phosphatase and tensin homolog (PTEN) gene deletion on RGCs stimulates both cell survival and axon regeneration (Benowitz et al., 2016 for review). The scenario revealed by these studies indicates that different mechanisms regulate RGC survival and axon regeneration. From these evidences, investigators started to combine different treatments, focusing on cell survival, axon regeneration, or both. The rationale behind this approach is that one would be able to stimulate both RGCs survival and axon regeneration at the same time, and possibly get additional effect after a lesion to the optic nerve. For instance, specific single treatments, such as conditional deletion of the PTEN gene in RGCs resulted in 45% of cell survival after optic nerve crush (ONC), and also promoted modest axon regeneration (Park et al., 2008). However, when combined with intraocular inflammation, a RGC survival rate of 54% was achieved as well as a 10 fold increase in axon regeneration, resulting in brain reinnervation (de Lima et al., 2012) (Figure 1E). Therefore, a combination of treatments can be a powerful tool to stimulate recovery of visual pathway. Thus, researchers are focusing their efforts on identifying potential candidates that can be more effective in one aspect (cell survival), in the other (axon regeneration), or both, so they can combine those candidates and boost brain target reinnervation.

Past, present and future of preserving and restoring function in the visual system: removing galectin-3 as a promising treatment