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

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...

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Published inFrontiers in neuroanatomy Vol. 16; p. 984052
Main Authors Martínez-Gil, Natalia, Maneu, Victoria, Kutsyr, Oksana, Fernández-Sánchez, Laura, Sánchez-Sáez, Xavier, Sánchez-Castillo, Carla, Campello, Laura, Lax, Pedro, Pinilla, Isabel, Cuenca, Nicolás
Format Journal Article
LanguageEnglish
Published Lausanne Frontiers Research Foundation 26.09.2022
Frontiers Media S.A
Subjects
Apoptosis
Cell death
cellular responses
Chemokines
Cytokines
Cytology
Disease
Energy metabolism
Gene expression
Glial cells
Gliosis
Inflammation
Kinases
Light effects
Metabolism
Morphology
Mutation
Neuroanatomy
Neurodegeneration
Neuronal-glial interactions
Neurons
Oxidative stress
Phenotypes
Photoreceptors
Proteins
reactive oxygen species
Retina
Retinal degeneration
Trophic factors
Online AccessGet full text
ISSN1662-5129
1662-5129
DOI10.3389/fnana.2022.984052

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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.
AbstractList 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.
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.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.
Multiple gene mutations have been associated with inherited retinal dystrophies (IRD). 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, reveals 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, with 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 in order 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.
Author Cuenca, Nicolás
Maneu, Victoria
Pinilla, Isabel
Fernández-Sánchez, Laura
Kutsyr, Oksana
Campello, Laura
Lax, Pedro
Sánchez-Sáez, Xavier
Martínez-Gil, Natalia
Sánchez-Castillo, Carla
AuthorAffiliation 1 Department of Physiology, Genetics and Microbiology, University of Alicante , Alicante , Spain
2 Department of Optics, Pharmacology and Anatomy, University of Alicante , Alicante , Spain
6 Department of Surgery, University of Zaragoza , Zaragoza , Spain
7 Institute Ramón Margalef, University of Alicante , Alicante , Spain
4 Aragón Institute for Health Research (IIS Aragón) , Zaragoza , Spain
5 Department of Ophthalmology, Lozano Blesa University Hospital , Zaragoza , Spain
3 Alicante Institute for Health and Biomedical Research (ISABIAL) , Alicante , Spain
AuthorAffiliation_xml – name: 5 Department of Ophthalmology, Lozano Blesa University Hospital , Zaragoza , Spain
– name: 2 Department of Optics, Pharmacology and Anatomy, University of Alicante , Alicante , Spain
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– name: 6 Department of Surgery, University of Zaragoza , Zaragoza , Spain
– name: 3 Alicante Institute for Health and Biomedical Research (ISABIAL) , Alicante , Spain
– name: 7 Institute Ramón Margalef, University of Alicante , Alicante , Spain
– name: 1 Department of Physiology, Genetics and Microbiology, University of Alicante , Alicante , Spain
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crossref_primary_10_1186_s12979_025_00502_2
crossref_primary_10_3390_biomedicines11102656
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Copyright © 2022 Martínez-Gil, Maneu, Kutsyr, Fernández-Sánchez, Sánchez-Sáez, Sánchez-Castillo, Campello, Lax, Pinilla and Cuenca.
Copyright © 2022 Martínez-Gil, Maneu, Kutsyr, Fernández-Sánchez, Sánchez-Sáez, Sánchez-Castillo, Campello, Lax, Pinilla and Cuenca. 2022 Martínez-Gil, Maneu, Kutsyr, Fernández-Sánchez, Sánchez-Sáez, Sánchez-Castillo, Campello, Lax, Pinilla and Cuenca
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Present address: Laura Campello, Neurobiology, Neurodegeneration and Repair Laboratory, National Eye Institute, National Institutes of Health, Bethesda, MD, United States
Reviewed by: Enrica Strettoi, Institute of Neuroscience (CNR), Italy; Hilda Petrs-Silva, Federal University of Rio de Janeiro, Brazil
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Snippet Multiple gene mutations have been associated with inherited retinal dystrophies (IRDs). Despite the spectrum of phenotypes caused by the distinct mutations,...
Multiple gene mutations have been associated with inherited retinal dystrophies (IRD). Despite the spectrum of phenotypes caused by the distinct mutations,...
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SubjectTerms Apoptosis
Cell death
cellular responses
Chemokines
Cytokines
Cytology
Disease
Energy metabolism
Gene expression
Glial cells
Gliosis
Inflammation
Kinases
Light effects
Metabolism
Morphology
Mutation
Neuroanatomy
Neurodegeneration
Neuronal-glial interactions
Neurons
Oxidative stress
Phenotypes
Photoreceptors
Proteins
reactive oxygen species
Retina
Retinal degeneration
Trophic factors
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Title Cellular and molecular alterations in neurons and glial cells in inherited retinal degeneration
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