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Título : Autophagy dysfunction and oxidative stress, two related mechanisms implicated in Retinitis Pigmentosa / Mari-Luz Moreno ... et al.
Autor : Moreno Sancho, María Luz.
Mérida Donoso, Salvador.
Bosch Morell, Francisco.
Miranda Sanz, María.
Villar Amigó, Vicente.
Materias: Retinitis pigmentosa - Treatment.Retina - Enfermedades - Tratamiento.Retina - Diseases - Treatment.Enfermedades genéticas - Tratamiento.Oxidative stress.Retinosis pigmentaria - Tratamiento.Mitocondrias - Fisiología.Mitochondria - Physiology.Estrés oxidativo.Genetic disorders - Treatment.
Fecha de publicación : 1-jul-2018
Citación : Moreno, ML., Mérida, S., Bosch Morell, F., Miranda, M. and Villar, VM. (2018). Autophagy dysfunction and oxidative stress, two related mechanisms implicated in Retinitis Pigmentosa. Frontiers in Physiology, vol. 9 (july), art. 1008. DOI: https://doi.org/10.3389/fphys.2018.01008
Resumen : Retinitis pigmentosa (RP) is one of the most common clinical subtypes of retinal degeneration (RD), and it is a neurodegenerative disease that could cause complete blindness in humans because it ultimately affects the photoreceptors viability. RP afflicts an estimated 1.5 million patients worldwide. The retina is highly susceptible to oxidative stress which can impair mitochondrial function. Many retina pathologies, such as diabetic retinopathy and secondary cone photoreceptor death in RP, have been related directly or indirectly with mitochondrial dysfunction. The possible role of autophagy in retina and cell differentiation is described and also the implications of autophagy dysregulation in RP. The present review shows the crucial role of autophagy in maintaining the retina homeostasis and possible therapeutic approaches for the treatment of RP.
Descripción : En Frontiers in Physiology. Lausanne (Suiza) : Frontiers Media. Vol. 9 (julio 2018), art. 1008.
Este artículo se encuentra disponible en la página web de la revista en la siguiente URL: https://www.frontiersin.org/articles/10.3389/fphys.2018.01008/full
URI : http://hdl.handle.net/10637/10231
Derechos: http://creativecommons.org/licenses/by/4.0/deed.es
ISSN : 1664-042X.
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