Mechanisms behind retinal ganglion cell loss in diabetes and therapeutic approach
- Autores
- Potilinski, María Constanza; Lorenc, Valeria Erika; Perisset, Sofía; Gallo, Juan Eduardo Maria
- Año de publicación
- 2020
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- Diabetes produces several changes in the body triggered by high glycemia. Some of these changes include altered metabolism, structural changes in blood vessels and chronic inflammation. The eye and particularly the retinal ganglion cells (RGCs) are not spared, and the changes eventually lead to cell loss and visual function impairment. Understanding the mechanisms resulting in RGC damage and loss from diabetic retinopathy is essential to find an effective treatment. This review focuses mainly on the signaling pathways and molecules involved in RGC loss and the potential therapeutic approaches for the prevention of this cell death. Throughout the manuscript it became evident that multiple factors of different kind are responsible for RGC damage. This shows that new therapeutic agents targeting several factors at the same time are needed. Alpha-1 antitrypsin as an anti-inflammatory agent may become a suitable option for the treatment of RGC loss because of its beneficial interaction with several signaling pathways involved in RGC injury and inflammation. In conclusion, alpha-1 antitrypsin may become a potential therapeutic agent for the treatment of RGC loss and processes behind diabetic retinopathy.
Fil: Potilinski, María Constanza. Universidad Austral. Facultad de Ciencias Biomédicas. Instituto de Investigaciones en Medicina Traslacional. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones en Medicina Traslacional; Argentina
Fil: Lorenc, Valeria Erika. Universidad Austral. Facultad de Ciencias Biomédicas. Instituto de Investigaciones en Medicina Traslacional. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones en Medicina Traslacional; Argentina
Fil: Perisset, Sofía. Universidad Austral. Facultad de Ciencias Biomédicas. Instituto de Investigaciones en Medicina Traslacional. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones en Medicina Traslacional; Argentina
Fil: Gallo, Juan Eduardo Maria. Universidad Austral. Facultad de Ciencias Biomédicas. Instituto de Investigaciones en Medicina Traslacional. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones en Medicina Traslacional; Argentina - Materia
-
ALPHA-1 ANTITRYPSIN
DIABETIC RETINOPATHY
INFLAMMATION
RETINAL GANGLION CELLS
SIGNALING PATHWAY - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by/2.5/ar/
- Repositorio
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/163885
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Mechanisms behind retinal ganglion cell loss in diabetes and therapeutic approachPotilinski, María ConstanzaLorenc, Valeria ErikaPerisset, SofíaGallo, Juan Eduardo MariaALPHA-1 ANTITRYPSINDIABETIC RETINOPATHYINFLAMMATIONRETINAL GANGLION CELLSSIGNALING PATHWAYhttps://purl.org/becyt/ford/3.4https://purl.org/becyt/ford/3Diabetes produces several changes in the body triggered by high glycemia. Some of these changes include altered metabolism, structural changes in blood vessels and chronic inflammation. The eye and particularly the retinal ganglion cells (RGCs) are not spared, and the changes eventually lead to cell loss and visual function impairment. Understanding the mechanisms resulting in RGC damage and loss from diabetic retinopathy is essential to find an effective treatment. This review focuses mainly on the signaling pathways and molecules involved in RGC loss and the potential therapeutic approaches for the prevention of this cell death. Throughout the manuscript it became evident that multiple factors of different kind are responsible for RGC damage. This shows that new therapeutic agents targeting several factors at the same time are needed. Alpha-1 antitrypsin as an anti-inflammatory agent may become a suitable option for the treatment of RGC loss because of its beneficial interaction with several signaling pathways involved in RGC injury and inflammation. In conclusion, alpha-1 antitrypsin may become a potential therapeutic agent for the treatment of RGC loss and processes behind diabetic retinopathy.Fil: Potilinski, María Constanza. Universidad Austral. Facultad de Ciencias Biomédicas. Instituto de Investigaciones en Medicina Traslacional. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones en Medicina Traslacional; ArgentinaFil: Lorenc, Valeria Erika. Universidad Austral. Facultad de Ciencias Biomédicas. Instituto de Investigaciones en Medicina Traslacional. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones en Medicina Traslacional; ArgentinaFil: Perisset, Sofía. Universidad Austral. Facultad de Ciencias Biomédicas. Instituto de Investigaciones en Medicina Traslacional. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones en Medicina Traslacional; ArgentinaFil: Gallo, Juan Eduardo Maria. Universidad Austral. Facultad de Ciencias Biomédicas. Instituto de Investigaciones en Medicina Traslacional. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones en Medicina Traslacional; ArgentinaMolecular Diversity Preservation International2020-03info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/163885Potilinski, María Constanza; Lorenc, Valeria Erika; Perisset, Sofía; Gallo, Juan Eduardo Maria; Mechanisms behind retinal ganglion cell loss in diabetes and therapeutic approach; Molecular Diversity Preservation International; International Journal of Molecular Sciences; 21; 7; 3-2020; 1-231422-0067CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.mdpi.com/1422-0067/21/7/2351info:eu-repo/semantics/altIdentifier/doi/10.3390/ijms21072351info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T09:40:41Zoai:ri.conicet.gov.ar:11336/163885instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-29 09:40:41.48CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
dc.title.none.fl_str_mv |
Mechanisms behind retinal ganglion cell loss in diabetes and therapeutic approach |
title |
Mechanisms behind retinal ganglion cell loss in diabetes and therapeutic approach |
spellingShingle |
Mechanisms behind retinal ganglion cell loss in diabetes and therapeutic approach Potilinski, María Constanza ALPHA-1 ANTITRYPSIN DIABETIC RETINOPATHY INFLAMMATION RETINAL GANGLION CELLS SIGNALING PATHWAY |
title_short |
Mechanisms behind retinal ganglion cell loss in diabetes and therapeutic approach |
title_full |
Mechanisms behind retinal ganglion cell loss in diabetes and therapeutic approach |
title_fullStr |
Mechanisms behind retinal ganglion cell loss in diabetes and therapeutic approach |
title_full_unstemmed |
Mechanisms behind retinal ganglion cell loss in diabetes and therapeutic approach |
title_sort |
Mechanisms behind retinal ganglion cell loss in diabetes and therapeutic approach |
dc.creator.none.fl_str_mv |
Potilinski, María Constanza Lorenc, Valeria Erika Perisset, Sofía Gallo, Juan Eduardo Maria |
author |
Potilinski, María Constanza |
author_facet |
Potilinski, María Constanza Lorenc, Valeria Erika Perisset, Sofía Gallo, Juan Eduardo Maria |
author_role |
author |
author2 |
Lorenc, Valeria Erika Perisset, Sofía Gallo, Juan Eduardo Maria |
author2_role |
author author author |
dc.subject.none.fl_str_mv |
ALPHA-1 ANTITRYPSIN DIABETIC RETINOPATHY INFLAMMATION RETINAL GANGLION CELLS SIGNALING PATHWAY |
topic |
ALPHA-1 ANTITRYPSIN DIABETIC RETINOPATHY INFLAMMATION RETINAL GANGLION CELLS SIGNALING PATHWAY |
purl_subject.fl_str_mv |
https://purl.org/becyt/ford/3.4 https://purl.org/becyt/ford/3 |
dc.description.none.fl_txt_mv |
Diabetes produces several changes in the body triggered by high glycemia. Some of these changes include altered metabolism, structural changes in blood vessels and chronic inflammation. The eye and particularly the retinal ganglion cells (RGCs) are not spared, and the changes eventually lead to cell loss and visual function impairment. Understanding the mechanisms resulting in RGC damage and loss from diabetic retinopathy is essential to find an effective treatment. This review focuses mainly on the signaling pathways and molecules involved in RGC loss and the potential therapeutic approaches for the prevention of this cell death. Throughout the manuscript it became evident that multiple factors of different kind are responsible for RGC damage. This shows that new therapeutic agents targeting several factors at the same time are needed. Alpha-1 antitrypsin as an anti-inflammatory agent may become a suitable option for the treatment of RGC loss because of its beneficial interaction with several signaling pathways involved in RGC injury and inflammation. In conclusion, alpha-1 antitrypsin may become a potential therapeutic agent for the treatment of RGC loss and processes behind diabetic retinopathy. Fil: Potilinski, María Constanza. Universidad Austral. Facultad de Ciencias Biomédicas. Instituto de Investigaciones en Medicina Traslacional. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones en Medicina Traslacional; Argentina Fil: Lorenc, Valeria Erika. Universidad Austral. Facultad de Ciencias Biomédicas. Instituto de Investigaciones en Medicina Traslacional. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones en Medicina Traslacional; Argentina Fil: Perisset, Sofía. Universidad Austral. Facultad de Ciencias Biomédicas. Instituto de Investigaciones en Medicina Traslacional. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones en Medicina Traslacional; Argentina Fil: Gallo, Juan Eduardo Maria. Universidad Austral. Facultad de Ciencias Biomédicas. Instituto de Investigaciones en Medicina Traslacional. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones en Medicina Traslacional; Argentina |
description |
Diabetes produces several changes in the body triggered by high glycemia. Some of these changes include altered metabolism, structural changes in blood vessels and chronic inflammation. The eye and particularly the retinal ganglion cells (RGCs) are not spared, and the changes eventually lead to cell loss and visual function impairment. Understanding the mechanisms resulting in RGC damage and loss from diabetic retinopathy is essential to find an effective treatment. This review focuses mainly on the signaling pathways and molecules involved in RGC loss and the potential therapeutic approaches for the prevention of this cell death. Throughout the manuscript it became evident that multiple factors of different kind are responsible for RGC damage. This shows that new therapeutic agents targeting several factors at the same time are needed. Alpha-1 antitrypsin as an anti-inflammatory agent may become a suitable option for the treatment of RGC loss because of its beneficial interaction with several signaling pathways involved in RGC injury and inflammation. In conclusion, alpha-1 antitrypsin may become a potential therapeutic agent for the treatment of RGC loss and processes behind diabetic retinopathy. |
publishDate |
2020 |
dc.date.none.fl_str_mv |
2020-03 |
dc.type.none.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion http://purl.org/coar/resource_type/c_6501 info:ar-repo/semantics/articulo |
format |
article |
status_str |
publishedVersion |
dc.identifier.none.fl_str_mv |
http://hdl.handle.net/11336/163885 Potilinski, María Constanza; Lorenc, Valeria Erika; Perisset, Sofía; Gallo, Juan Eduardo Maria; Mechanisms behind retinal ganglion cell loss in diabetes and therapeutic approach; Molecular Diversity Preservation International; International Journal of Molecular Sciences; 21; 7; 3-2020; 1-23 1422-0067 CONICET Digital CONICET |
url |
http://hdl.handle.net/11336/163885 |
identifier_str_mv |
Potilinski, María Constanza; Lorenc, Valeria Erika; Perisset, Sofía; Gallo, Juan Eduardo Maria; Mechanisms behind retinal ganglion cell loss in diabetes and therapeutic approach; Molecular Diversity Preservation International; International Journal of Molecular Sciences; 21; 7; 3-2020; 1-23 1422-0067 CONICET Digital CONICET |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
info:eu-repo/semantics/altIdentifier/url/https://www.mdpi.com/1422-0067/21/7/2351 info:eu-repo/semantics/altIdentifier/doi/10.3390/ijms21072351 |
dc.rights.none.fl_str_mv |
info:eu-repo/semantics/openAccess https://creativecommons.org/licenses/by/2.5/ar/ |
eu_rights_str_mv |
openAccess |
rights_invalid_str_mv |
https://creativecommons.org/licenses/by/2.5/ar/ |
dc.format.none.fl_str_mv |
application/pdf application/pdf application/pdf application/pdf |
dc.publisher.none.fl_str_mv |
Molecular Diversity Preservation International |
publisher.none.fl_str_mv |
Molecular Diversity Preservation International |
dc.source.none.fl_str_mv |
reponame:CONICET Digital (CONICET) instname:Consejo Nacional de Investigaciones Científicas y Técnicas |
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CONICET Digital (CONICET) |
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CONICET Digital (CONICET) |
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Consejo Nacional de Investigaciones Científicas y Técnicas |
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CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas |
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dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar |
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13.070432 |