• Login
    View Item 
    •   Home
    • Centers & Institutes
    • James and Jean Culver Vision Discovery Institute
    • James and Jean Culver Vision Discovery Institute: Faculty Research and Publications
    • View Item
    •   Home
    • Centers & Institutes
    • James and Jean Culver Vision Discovery Institute
    • James and Jean Culver Vision Discovery Institute: Faculty Research and Publications
    • View Item
    JavaScript is disabled for your browser. Some features of this site may not work without it.

    Browse

    All of Scholarly CommonsCommunitiesTitleAuthorsIssue DateSubmit DateSubjectsThis CollectionTitleAuthorsIssue DateSubmit DateSubjects

    My Account

    LoginRegister

    About

    AboutCreative CommonsAugusta University LibrariesUSG Copyright Policy

    Statistics

    Display statistics

    Alteration of growth factors and neuronal death in diabetic retinopathy: what we have learned so far

    • CSV
    • RefMan
    • EndNote
    • BibTex
    • RefWorks
    Thumbnail
    Name:
    mv-v17-300.pdf
    Size:
    373.4Kb
    Format:
    PDF
    Download
    Authors
    Whitmire, Will
    Al-Gayyar, Mohammed M H
    Abdelsaid, Mohammed
    Yousufzai, Bilal K
    El-Remessy, Azza B.
    Issue Date
    2011-01-28
    URI
    http://hdl.handle.net/10675.2/634
    
    Metadata
    Show full item record
    Abstract
    Purpose: Diabetic retinopathy (DR) is a leading cause of blindness in American adults. Over the years, DR has been perceived as a vascular disease characterized by vascular permeability, macular edema, and neovascularization that can lead to blindness. Relatively new research on neurodegeneration is expanding our views of the pathogenesis of DR. Evidence has begun to point to the fact that even before vascular complications begin to manifest, neuronal cell death and dysfunction have already begun. Based on the literature and our own studies, we address whether neuronal death is associated with loss of neurotrophic support due to less production of a given growth factor or due to impairment of its signaling events regardless of the level of the growth factor itself.
    Methods: In this article we aimed to review the literature that looks at the neuronal side of DR and whether retinal neurons are adversely affected due to the lack of neurotrophic levels or activity. In particular, we examine the research looking at insulin, insulin-like growth factor, vascular endothelial growth factor, pigment epithelium-derived growth factor, brain-derived neurotrophic factor, and nerve growth factor.
    Results: Research shows that insulin has neurotrophic properties and that the loss of its pro-survival pathways may have a role in diabetic retinopathy. There is also evidence to suggest that exogenously administered insulin may have a role in the treatment of DR. Insulin-like growth factor has been shown to have a role in retinal neurogenesis and there is early evidence that it may also have neuroprotective effects. While there is evidence of neuroprotective effects of vascular endothelial growth factor, paradoxically, there is also an increased amount of apoptotic activity in retinal neurons despite an increased level of VEGF in the diabetic eye. Further research is necessary to elucidate the exact mechanisms involved. Pigment epithelium derived growth factor has retinal neuroprotective effects and shows evidence that it may be an avenue for future therapeutic use in DR. Brain-derived growth factor has been shown to have neuroprotective effects in the retina and there is also some evidence in diabetic rats that it may have some therapeutic potential in treating DR. Nerve growth factor has also been shown to have neuroprotective effects and research has begun to elucidate some of the pathways and mechanisms through which these effects occur.
    Conclusions: Research has shown that there is some degree of neuronal death involved in DR. It is also evident that there are many growth factors involved in this process. Some of these growth factors have shown some potential as future therapeutic targets in DR. These findings should encourage further investigation into the mechanism of these growth factors, their potential for therapy, and the possibility of a new horizon in the clinical care of DR.
    Citation
    Mol Vis. 2011 Jan 28; 17:300-308
    Collections
    James and Jean Culver Vision Discovery Institute: Faculty Research and Publications

    entitlement

    Related articles

    • Long-term retinal PEDF overexpression prevents neovascularization in a murine adult model of retinopathy.
    • Authors: Haurigot V, Villacampa P, Ribera A, Bosch A, Ramos D, Ruberte J, Bosch F
    • Issue date: 2012
    • Unbalanced vitreous levels of pigment epithelium-derived factor and vascular endothelial growth factor in diabetic retinopathy.
    • Authors: Ogata N, Nishikawa M, Nishimura T, Mitsuma Y, Matsumura M
    • Issue date: 2002 Sep
    • Pigment epithelium-derived factor downregulates vascular endothelial growth factor (VEGF) expression and inhibits VEGF-VEGF receptor 2 binding in diabetic retinopathy.
    • Authors: Zhang SX, Wang JJ, Gao G, Parke K, Ma JX
    • Issue date: 2006 Aug
    • Pigment epithelium-derived factor (PEDF) is an endogenous antiinflammatory factor.
    • Authors: Zhang SX, Wang JJ, Gao G, Shao C, Mott R, Ma JX
    • Issue date: 2006 Feb
    • A Review: Proteomics in Retinal Artery Occlusion, Retinal Vein Occlusion, Diabetic Retinopathy and Acquired Macular Disorders.
    • Authors: Cehofski LJ, Honoré B, Vorum H
    • Issue date: 2017 Apr 28
    DSpace software (copyright © 2002 - 2023)  DuraSpace
    Quick Guide | Contact Us
    Open Repository is a service operated by 
    Atmire NV
     

    Export search results

    The export option will allow you to export the current search results of the entered query to a file. Different formats are available for download. To export the items, click on the button corresponding with the preferred download format.

    By default, clicking on the export buttons will result in a download of the allowed maximum amount of items.

    To select a subset of the search results, click "Selective Export" button and make a selection of the items you want to export. The amount of items that can be exported at once is similarly restricted as the full export.

    After making a selection, click one of the export format buttons. The amount of items that will be exported is indicated in the bubble next to export format.