[Update on retinal transplantation and its clinical limitations].


EDITORIAL At present, cellular and genetic therapies constitute realistic approaches for the treatment of neuro-degenerative retina diseases. Developments in genetic science have provided a new vision of the physiology and pathogenesis of specific genetically-induced retinal diseases and potential treatments thereof through the modification of the genes involved. Although considerable progress has been made in treatments on animal models (as well as in clinical experimentation phases) for some pathologies such as Leber's congenital amaurosis, gene therapy doesn't appear to be an option in patients with important visual loss derived from loss of photoreceptors or retinal pigmentary epithelium cells (RPE) which have caused large-scale changes in retinal circuits (1,2). The use of said treatments is also difficult in pat-hologies comprising a large amount of ethiopatho-genic factors, such as Age-Related Macular Dege-neration, with the additional drawback of its high cost in diseases where researchers continue to discover a vast amount of genes involved in the patho-geny thereof, for instance Pigmentary Retinosis. The possibility of re-establishing eyesight was the purpose of initial research into retinal transplan-tations performed at the brain level, which proved that the transplant had the capacity of axonal growth and establishment of synapses and physiological responses (3). In the light of said results, it was easy to think that if the transplantation was made at the sub-reti-nal level, the cells involved would be able to establish new synaptic connections and develop functional capacities. There are two different approaches to retinal transplantations: the first is based on limiting the loss of photoreceptors by introducing cells to maintain their function, and the second option is replacing the photoreceptors which have been lost. Both options share some problems, like selecting the right type of cells, the transplantation method (isolated cells or full tissue), how to minimize postop inflammatory reactions and immune responses, selecting the method for performing the transplan-tation, the optimization of its efficiency and postop success assessment. The selection of the type of cell will depend on the cause of photoreceptor loss. If the disease originated in RPE defects, this type of cell or others can be injected to improve the chemical environment at the sub-retinal space. The range of cells utilized for this purpose include RPE cells, iris pigmented cells or immortalized cells, improving cell survival as well as achieving the preservation of its functions (4,5). For improving the cellular environment, growth factors or neurotrophines have been injected, growth factor-secreting cells (such …

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@article{Pinilla2006UpdateOR, title={[Update on retinal transplantation and its clinical limitations].}, author={Isabel Pinilla and Nicol{\'a}s Cuenca}, journal={Archivos de la Sociedad Española de Oftalmología}, year={2006}, volume={81 5}, pages={239-40} }