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Diabetes and retinal vascular dysfunction.

Shin ES, Sorenson CM, Sheibani N - J Ophthalmic Vis Res (2014 Jul-Sep)

Bottom Line: These changes ultimately lead to altered permeability, hyperproliferation of endothelial cells and edema, and abnormal vascularization of the retina with resulting loss of vision.Enhanced production of inflammatory mediators and oxidative stress are primary insults with significant contribution to the pathogenesis of diabetic retinopathy (DR).This knowledge provides novel insight into the molecular and cellular defects contributing to the development and progression of diabetic retinopathy, and will aid in the development of innovative, as well as target specific therapeutic approaches for prevention and treatment of DR.

View Article: PubMed Central - PubMed

Affiliation: Department of Ophthalmology and Visual Sciences, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.

ABSTRACT
Diabetes predominantly affects the microvascular circulation of the retina resulting in a range of structural changes unique to this tissue. These changes ultimately lead to altered permeability, hyperproliferation of endothelial cells and edema, and abnormal vascularization of the retina with resulting loss of vision. Enhanced production of inflammatory mediators and oxidative stress are primary insults with significant contribution to the pathogenesis of diabetic retinopathy (DR). We have determined the identity of the retinal vascular cells affected by hyperglycemia, and have delineated the cell autonomous impact of high glucose on function of these cells. We discuss some of the high glucose specific changes in retinal vascular cells and their contribution to retinal vascular dysfunction. This knowledge provides novel insight into the molecular and cellular defects contributing to the development and progression of diabetic retinopathy, and will aid in the development of innovative, as well as target specific therapeutic approaches for prevention and treatment of DR.

No MeSH data available.


Related in: MedlinePlus

Vascular changes in diabetic retina. Pericytes control vessel stability and proliferation of endothelial cells. Pericyte loss contributes to breakdown of blood-retinal barrier (BRB) and damage to the endothelium, and formation of acellular capillaries. These vascular changes caused by pericyte loss lead to ischemia, proliferative vascularization of retina, and retinal detachment and loss of vision.
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Figure 2: Vascular changes in diabetic retina. Pericytes control vessel stability and proliferation of endothelial cells. Pericyte loss contributes to breakdown of blood-retinal barrier (BRB) and damage to the endothelium, and formation of acellular capillaries. These vascular changes caused by pericyte loss lead to ischemia, proliferative vascularization of retina, and retinal detachment and loss of vision.

Mentions: In the diabetic retina, nonperfused and obliterated microvessels are observed in the early stages of retinopathy. Vessel closure promotes the proliferative retinal neovascularization and can be histologically observed as the prevalence of acellular capillaries increases.[60] Adhesion of leukocyte to the retinal blood vessel induces endothelial cell death, pericyte loss and vascular closure leading to ischemia[12] which is the primary stimulus for neovascularization.[61] Leukocyte adhesion to retinal vessels is mediated by ICAM-1 and vascular cellular adhesion molecule-1.[62] The activation of neovascularization is mediated by hypoxia-inducible factor 1-alpha (HIF-1α) which is a transcription factor and regulates the expression of various pro-angiogenic genes including VEGF, VEGF receptor-1, and angiopoietin-1 (Ang-1).[63] Aberrant activation of these pro-angiogenic factors under diabetic conditions results in pathological neovascularization. Thus, vascular changes in the diabetic retina promote the breakdown of BRB, macular edema, and proliferative neovascularization leading to retinal detachment and impairment of vision [Figure 2].


Diabetes and retinal vascular dysfunction.

Shin ES, Sorenson CM, Sheibani N - J Ophthalmic Vis Res (2014 Jul-Sep)

Vascular changes in diabetic retina. Pericytes control vessel stability and proliferation of endothelial cells. Pericyte loss contributes to breakdown of blood-retinal barrier (BRB) and damage to the endothelium, and formation of acellular capillaries. These vascular changes caused by pericyte loss lead to ischemia, proliferative vascularization of retina, and retinal detachment and loss of vision.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4307665&req=5

Figure 2: Vascular changes in diabetic retina. Pericytes control vessel stability and proliferation of endothelial cells. Pericyte loss contributes to breakdown of blood-retinal barrier (BRB) and damage to the endothelium, and formation of acellular capillaries. These vascular changes caused by pericyte loss lead to ischemia, proliferative vascularization of retina, and retinal detachment and loss of vision.
Mentions: In the diabetic retina, nonperfused and obliterated microvessels are observed in the early stages of retinopathy. Vessel closure promotes the proliferative retinal neovascularization and can be histologically observed as the prevalence of acellular capillaries increases.[60] Adhesion of leukocyte to the retinal blood vessel induces endothelial cell death, pericyte loss and vascular closure leading to ischemia[12] which is the primary stimulus for neovascularization.[61] Leukocyte adhesion to retinal vessels is mediated by ICAM-1 and vascular cellular adhesion molecule-1.[62] The activation of neovascularization is mediated by hypoxia-inducible factor 1-alpha (HIF-1α) which is a transcription factor and regulates the expression of various pro-angiogenic genes including VEGF, VEGF receptor-1, and angiopoietin-1 (Ang-1).[63] Aberrant activation of these pro-angiogenic factors under diabetic conditions results in pathological neovascularization. Thus, vascular changes in the diabetic retina promote the breakdown of BRB, macular edema, and proliferative neovascularization leading to retinal detachment and impairment of vision [Figure 2].

Bottom Line: These changes ultimately lead to altered permeability, hyperproliferation of endothelial cells and edema, and abnormal vascularization of the retina with resulting loss of vision.Enhanced production of inflammatory mediators and oxidative stress are primary insults with significant contribution to the pathogenesis of diabetic retinopathy (DR).This knowledge provides novel insight into the molecular and cellular defects contributing to the development and progression of diabetic retinopathy, and will aid in the development of innovative, as well as target specific therapeutic approaches for prevention and treatment of DR.

View Article: PubMed Central - PubMed

Affiliation: Department of Ophthalmology and Visual Sciences, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.

ABSTRACT
Diabetes predominantly affects the microvascular circulation of the retina resulting in a range of structural changes unique to this tissue. These changes ultimately lead to altered permeability, hyperproliferation of endothelial cells and edema, and abnormal vascularization of the retina with resulting loss of vision. Enhanced production of inflammatory mediators and oxidative stress are primary insults with significant contribution to the pathogenesis of diabetic retinopathy (DR). We have determined the identity of the retinal vascular cells affected by hyperglycemia, and have delineated the cell autonomous impact of high glucose on function of these cells. We discuss some of the high glucose specific changes in retinal vascular cells and their contribution to retinal vascular dysfunction. This knowledge provides novel insight into the molecular and cellular defects contributing to the development and progression of diabetic retinopathy, and will aid in the development of innovative, as well as target specific therapeutic approaches for prevention and treatment of DR.

No MeSH data available.


Related in: MedlinePlus