Mitochondrial Dysfunction and Endoplasmic Reticulum Stress in Age Related Macular Degeneration, Role in Pathophysiology, and Possible New Therapeutic Strategies
Valentina Bilbao-Malavé,
Jorge González-Zamora,
Miriam de la Puente,
Sergio Recalde,
Patricia Fernandez-Robredo,
María Hernandez,
Alfredo Garcia Layana,
Manuel Saenz de Viteri
Affiliations
Valentina Bilbao-Malavé
Department of Opthalmology, Clínica Universidad de Navarra, 31008 Pamplona, Spain
Jorge González-Zamora
Department of Opthalmology, Clínica Universidad de Navarra, 31008 Pamplona, Spain
Miriam de la Puente
Department of Opthalmology, Clínica Universidad de Navarra, 31008 Pamplona, Spain
Sergio Recalde
Retinal Pathologies and New Therapies Group, Experimental Ophthalmology Laboratory, Department of Ophthalmology, Universidad de Navarra, 31008 Pamplona, Spain
Patricia Fernandez-Robredo
Retinal Pathologies and New Therapies Group, Experimental Ophthalmology Laboratory, Department of Ophthalmology, Universidad de Navarra, 31008 Pamplona, Spain
María Hernandez
Retinal Pathologies and New Therapies Group, Experimental Ophthalmology Laboratory, Department of Ophthalmology, Universidad de Navarra, 31008 Pamplona, Spain
Alfredo Garcia Layana
Department of Opthalmology, Clínica Universidad de Navarra, 31008 Pamplona, Spain
Manuel Saenz de Viteri
Department of Opthalmology, Clínica Universidad de Navarra, 31008 Pamplona, Spain
Age related macular degeneration (AMD) is the main cause of legal blindness in developed countries. It is a multifactorial disease in which a combination of genetic and environmental factors contributes to increased risk of developing this vision-incapacitating condition. Oxidative stress plays a central role in the pathophysiology of AMD and recent publications have highlighted the importance of mitochondrial dysfunction and endoplasmic reticulum stress in this disease. Although treatment with vascular endothelium growth factor inhibitors have decreased the risk of blindness in patients with the exudative form of AMD, the search for new therapeutic options continues to prevent the loss of photoreceptors and retinal pigment epithelium cells, characteristic of late stage AMD. In this review, we explain how mitochondrial dysfunction and endoplasmic reticulum stress participate in AMD pathogenesis. We also discuss a role of several antioxidants (bile acids, resveratrol, melatonin, humanin, and coenzyme Q10) in amelioration of AMD pathology.
