title: Cellular responses following retinal injuries and therapeutic approaches for neurodegenerative diseases.
abstract: Retinal neurodegenerative diseases like age-related macular degeneration, glaucoma, diabetic retinopathy and retinitis pigmentosa each have a different etiology and pathogenesis. However, at the cellular and molecular level, the response to retinal injury is similar in all of them, and results in morphological and functional impairment of retinal cells. This retinal degeneration may be triggered by gene defects, increased intraocular pressure, high levels of blood glucose, other types of stress or aging, but they all frequently induce a set of cell signals that lead to well-established and similar morphological and functional changes, including controlled cell death and retinal remodeling. Interestingly, an inflammatory response, oxidative stress and activation of apoptotic pathways are common features in all these diseases. Furthermore, it is important to note the relevant role of glial cells, including astrocytes, Müller cells and microglia, because their response to injury is decisive for maintaining the health of the retina or its degeneration. Several therapeutic approaches have been developed to preserve retinal function or restore eyesight in pathological conditions. In this context, neuroprotective compounds, gene therapy, cell transplantation or artificial devices should be applied at the appropriate stage of retinal degeneration to obtain successful results. This review provides an overview of the common and distinctive features of retinal neurodegenerative diseases, including the molecular, anatomical and functional changes caused by the cellular response to damage, in order to establish appropriate treatments for these pathologies.
authors.affiliation: Department of Physiology, Genetics and Microbiology, University of Alicante, Alicante, Spain; Multidisciplinary Institute for Environmental Studies "Ramon Margalef", University of Alicante, Alicante, Spain. Electronic address: cuenca@ua.es.
authors.forename: Nicolás
authors.initials: N
authors.lastname: Cuenca
authors.affiliation: Department of Physiology, Genetics and Microbiology, University of Alicante, Alicante, Spain.
authors.forename: Laura
authors.initials: L
authors.lastname: Fernández-Sánchez
authors.affiliation: Department of Physiology, Genetics and Microbiology, University of Alicante, Alicante, Spain.
authors.forename: Laura
authors.initials: L
authors.lastname: Campello
authors.affiliation: Department of Optics, Pharmacology and Anatomy, University of Alicante, Alicante, Spain.
authors.forename: Victoria
authors.initials: V
authors.lastname: Maneu
authors.affiliation: Department of Systems Biology, University of Alcalá, Alcalá de Henares, Spain.
authors.forename: Pedro
authors.initials: P
authors.lastname: De la Villa
authors.affiliation: Department of Physiology, Genetics and Microbiology, University of Alicante, Alicante, Spain.
authors.forename: Pedro
authors.initials: P
authors.lastname: Lax
authors.affiliation: Department of Ophthalmology, Lozano Blesa University Hospital, Aragon Institute of Health Sciences, Zaragoza, Spain.
authors.forename: Isabel
authors.initials: I
authors.lastname: Pinilla
mesh_terms: D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D000975:Antioxidants / Q000627:therapeutic use; D017209:Apoptosis / Q000502:physiology; D002986:Clinical Trials as Topic; D006801:Humans; D019636:Neurodegenerative Diseases / Q000503:physiopathology / Q000628:therapy; D018696:Neuroprotective Agents / Q000627:therapeutic use; D018384:Oxidative Stress / Q000502:physiology; D012162:Retinal Degeneration / Q000503:physiopathology / Q000628:therapy; D055351:Retinal Neurons / Q000473:pathology / Q000502:physiology; D033581:Stem Cell Transplantation / Q000379:methods
chemical_list: D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D018696:Neuroprotective Agents
keywords: Glial cells; Neurodegeneration; Neuroprotection; Retinal diseases; Retinal remodeling; Retinal therapy