Cellular and molecular alterations in neurons and glial cells in inherited retinal degeneration

Please use this identifier to cite or link to this item: http://hdl.handle.net/10045/127982
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Title: Cellular and molecular alterations in neurons and glial cells in inherited retinal degeneration
Authors: Martínez Gil, Natalia | Maneu, Victoria | Kutsyr, Oksana | Fernández-Sánchez, Laura | Sánchez-Sáez, Xavier | Sánchez-Castillo, Carla | Campello Blasco, Laura | Lax, Pedro | Pinilla Lozano, Isabel | Cuenca, Nicolás
Research Group/s: Neurobiología del Sistema Visual y Terapia de Enfermedades Neurodegenerativas (NEUROVIS)
Center, Department or Service: Universidad de Alicante. Departamento de Fisiología, Genética y Microbiología | Universidad de Alicante. Departamento de Óptica, Farmacología y Anatomía | Universidad de Alicante. Instituto Multidisciplinar para el Estudio del Medio "Ramón Margalef"
Keywords: Retinal degeneration | Cellular responses | Oxidative stress | Inflammation | Reactive oxygen species
Issue Date: 26-Sep-2022
Publisher: Frontiers Media
Citation: Martínez-Gil N, Maneu V, Kutsyr O, Fernández-Sánchez L, Sánchez-Sáez X, Sánchez-Castillo C, Campello L, Lax P, Pinilla I and Cuenca N (2022) Cellular and molecular alterations in neurons and glial cells in inherited retinal degeneration. Front. Neuroanat. 16:984052. doi: 10.3389/fnana.2022.984052
Abstract: Multiple gene mutations have been associated with inherited retinal dystrophies (IRDs). Despite the spectrum of phenotypes caused by the distinct mutations, IRDs display common physiopathology features. Cell death is accompanied by inflammation and oxidative stress. The vertebrate retina has several attributes that make this tissue vulnerable to oxidative and nitrosative imbalance. The high energy demands and active metabolism in retinal cells, as well as their continuous exposure to high oxygen levels and light-induced stress, reveal the importance of tightly regulated homeostatic processes to maintain retinal function, which are compromised in pathological conditions. In addition, the subsequent microglial activation and gliosis, which triggers the secretion of pro-inflammatory cytokines, chemokines, trophic factors, and other molecules, further worsen the degenerative process. As the disease evolves, retinal cells change their morphology and function. In disease stages where photoreceptors are lost, the remaining neurons of the retina to preserve their function seek out for new synaptic partners, which leads to a cascade of morphological alterations in retinal cells that results in a complete remodeling of the tissue. In this review, we describe important molecular and morphological changes in retinal cells that occur in response to oxidative stress and the inflammatory processes underlying IRDs.
Sponsor: This research was funded by the DGA group B08_17R: Investigación en Retina y Sistema Visual and Fondo Europeo de Desarrollo Regional (FEDER) funds: “Una manera de hacer Europa”, Ministerio de Ciencia e Innovación (FEDER-PID 2019-106230RB-I00), Instituto de Salud Carlos III (PI20/00740-FEDER, RETICS-FEDER RD16/0008/0016), Generalitat Valenciana-FEDER (IDIFEDER/2017/064, PROMETEO/2021/024), Ministerio de Universidades (FPU16/04114), Es Retina Asturias (2019/00286/001). The APC was funded by the DGA group B08_17R: Investigación en Retina y Sistema Visual (FEDER).
URI: http://hdl.handle.net/10045/127982
ISSN: 1662-5129
DOI: 10.3389/fnana.2022.984052
Language: eng
Type: info:eu-repo/semantics/article
Rights: © 2022 Martínez-Gil, Maneu, Kutsyr, Fernández-Sánchez, Sánchez-Sáez, Sánchez-Castillo, Campello, Lax, Pinilla and Cuenca. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
Peer Review: si
Publisher version: https://doi.org/10.3389/fnana.2022.984052
Appears in Collections:INV - NEUROVIS - Artículos de Revistas

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