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Endothelial Progenitor Cells in Diabetic Retinopathy
Diabetic retinopathy (DR) is a leading cause of visual impairment worldwide. Patients with DR may irreversibly lose sight as a result of the development of diabetic macular edema (DME) and/or proliferative diabetic retinopathy (PDR); retinal blood vessel dysfunction and degeneration plays an essenti...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2014
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3988370/ https://www.ncbi.nlm.nih.gov/pubmed/24782825 http://dx.doi.org/10.3389/fendo.2014.00044 |
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author | Lois, Noemi McCarter, Rachel V. O’Neill, Christina Medina, Reinhold J. Stitt, Alan W. |
author_facet | Lois, Noemi McCarter, Rachel V. O’Neill, Christina Medina, Reinhold J. Stitt, Alan W. |
author_sort | Lois, Noemi |
collection | PubMed |
description | Diabetic retinopathy (DR) is a leading cause of visual impairment worldwide. Patients with DR may irreversibly lose sight as a result of the development of diabetic macular edema (DME) and/or proliferative diabetic retinopathy (PDR); retinal blood vessel dysfunction and degeneration plays an essential role in their pathogenesis. Although new treatments have been recently introduced for DME, including intravitreal vascular endothelial growth factor inhibitors (anti-VEGFs) and steroids, a high proportion of patients (~40–50%) do not respond to these therapies. Furthermore, for people with PDR, laser photocoagulation remains a mainstay therapy despite this being an inherently destructive procedure. Endothelial progenitor cells (EPCs) are a low-frequency population of circulating cells known to be recruited to sites of vessel damage and tissue ischemia where they promote vascular healing and re-perfusion. A growing body of evidence suggests that the number and function of EPCs are altered in patients with varying degrees of diabetes duration, metabolic control, and in the presence or absence of DR. Although there are no clear-cut outcomes from these clinical studies, there is mounting evidence that some EPC sub-types may be involved in the pathogenesis of DR and may also serve as biomarkers for disease progression and stratification. Moreover, some EPC sub-types have considerable potential as therapeutic modalities for DME and PDR in the context of cell therapy. This study presents basic clinical concepts of DR and combines this with a general insight on EPCs and their relation to future directions in understanding and treating this important diabetic complication. |
format | Online Article Text |
id | pubmed-3988370 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-39883702014-04-29 Endothelial Progenitor Cells in Diabetic Retinopathy Lois, Noemi McCarter, Rachel V. O’Neill, Christina Medina, Reinhold J. Stitt, Alan W. Front Endocrinol (Lausanne) Endocrinology Diabetic retinopathy (DR) is a leading cause of visual impairment worldwide. Patients with DR may irreversibly lose sight as a result of the development of diabetic macular edema (DME) and/or proliferative diabetic retinopathy (PDR); retinal blood vessel dysfunction and degeneration plays an essential role in their pathogenesis. Although new treatments have been recently introduced for DME, including intravitreal vascular endothelial growth factor inhibitors (anti-VEGFs) and steroids, a high proportion of patients (~40–50%) do not respond to these therapies. Furthermore, for people with PDR, laser photocoagulation remains a mainstay therapy despite this being an inherently destructive procedure. Endothelial progenitor cells (EPCs) are a low-frequency population of circulating cells known to be recruited to sites of vessel damage and tissue ischemia where they promote vascular healing and re-perfusion. A growing body of evidence suggests that the number and function of EPCs are altered in patients with varying degrees of diabetes duration, metabolic control, and in the presence or absence of DR. Although there are no clear-cut outcomes from these clinical studies, there is mounting evidence that some EPC sub-types may be involved in the pathogenesis of DR and may also serve as biomarkers for disease progression and stratification. Moreover, some EPC sub-types have considerable potential as therapeutic modalities for DME and PDR in the context of cell therapy. This study presents basic clinical concepts of DR and combines this with a general insight on EPCs and their relation to future directions in understanding and treating this important diabetic complication. Frontiers Media S.A. 2014-04-09 /pmc/articles/PMC3988370/ /pubmed/24782825 http://dx.doi.org/10.3389/fendo.2014.00044 Text en Copyright © 2014 Lois, McCarter, O’Neill, Medina and Stitt. http://creativecommons.org/licenses/by/3.0/ 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) or licensor 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. |
spellingShingle | Endocrinology Lois, Noemi McCarter, Rachel V. O’Neill, Christina Medina, Reinhold J. Stitt, Alan W. Endothelial Progenitor Cells in Diabetic Retinopathy |
title | Endothelial Progenitor Cells in Diabetic Retinopathy |
title_full | Endothelial Progenitor Cells in Diabetic Retinopathy |
title_fullStr | Endothelial Progenitor Cells in Diabetic Retinopathy |
title_full_unstemmed | Endothelial Progenitor Cells in Diabetic Retinopathy |
title_short | Endothelial Progenitor Cells in Diabetic Retinopathy |
title_sort | endothelial progenitor cells in diabetic retinopathy |
topic | Endocrinology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3988370/ https://www.ncbi.nlm.nih.gov/pubmed/24782825 http://dx.doi.org/10.3389/fendo.2014.00044 |
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