Autophagy Dysfunction and Oxidative Stress, Two Related Mechanisms Implicated in Retinitis Pigmentosa


Por: Moreno ML, Mérida S, Bosch-Morell F, Miranda M and Villar VM

Publicada: 26 jul 2018
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.

Filiaciones:
Moreno ML:
 Department of Basic Sciences, Universidad Católica de Valencia San Vicente Mártir, Valencia, Spain

Mérida S:
 Departamento de Ciencias Biomédicas, Facultad de Ciencias de la Salud, Universidad Cardenal Herrera-CEU, CEU Universities, Valencia, Spain

:
 Departamento de Ciencias Biomédicas, Facultad de Ciencias de la Salud, Universidad Cardenal Herrera-CEU, CEU Universities, Valencia, Spain

 Department of Medical Ophtalmology, Fundación para el Fomento de la Investigación Sanitaria y Biomédica de la Comunitat Valenciana, Valencia, Spain

Miranda M:
 Departamento de Ciencias Biomédicas, Facultad de Ciencias de la Salud, Universidad Cardenal Herrera-CEU, CEU Universities, Valencia, Spain

Villar VM:
 Departamento de Ciencias Biomédicas, Facultad de Ciencias de la Salud, Universidad Cardenal Herrera-CEU, CEU Universities, Valencia, Spain
ISSN: 1664042X





Frontiers in Physiology
Editorial
Frontiers Media S.A., AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND, Suiza
Tipo de documento: Review
Volumen: 9 Número:
Páginas: 1008-1008
WOS Id: 000439883900002
ID de PubMed: 30093867

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