Defining Diabetic Retinopathy Severity

Wong, Keye

doi:10.1007/978-0-387-85900-2_5

Cited by 6 publications

(2 citation statements)

References 23 publications

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“…Additionally retina on one side of a bounding retinal arteriole or venule may be completely lacking in capillaries whereas that on the other side sometimes possesses an intact capillary network ( Fig 1B ). This sort of pattern occurs both in the peripheral retina and also between the arterioles and venules supplying the fovea (Figure 6.16 P 136, [ 24 ]).…”

Section: Introductionmentioning

confidence: 99%

Progression of Diabetic Capillary Occlusion: A Model

Gens

Glazier

et al. 2016

PLoS Comput Biol

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An explanatory computational model is developed of the contiguous areas of retinal capillary loss which play a large role in diabetic maculapathy and diabetic retinal neovascularization. Strictly random leukocyte mediated capillary occlusion cannot explain the occurrence of large contiguous areas of retinal ischemia. Therefore occlusion of an individual capillary must increase the probability of occlusion of surrounding capillaries. A retinal perifoveal vascular sector as well as a peripheral retinal capillary network and a deleted hexagonal capillary network are modelled using Compucell3D. The perifoveal modelling produces a pattern of spreading capillary loss with associated macular edema. In the peripheral network, spreading ischemia results from the progressive loss of the ladder capillaries which connect peripheral arterioles and venules. System blood flow was elevated in the macular model before a later reduction in flow in cases with progression of capillary occlusions. Simulations differing only in initial vascular network structures but with identical dynamics for oxygen, growth factors and vascular occlusions, replicate key clinical observations of ischemia and macular edema in the posterior pole and ischemia in the retinal periphery. The simulation results also seem consistent with quantitative data on macular blood flow and qualitative data on venous oxygenation. One computational model applied to distinct capillary networks in different retinal regions yielded results comparable to clinical observations in those regions.

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Section: Introductionmentioning

confidence: 99%

Progression of Diabetic Capillary Occlusion: A Model

Gens

Glazier

et al. 2016

PLoS Comput Biol

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“…Although DR influence all retinal cells, clinical manifestations of DR are mainly due to changes in retinal vessels, where early histological alterations include pericyte loss, thickening of basement membrane, capillary occlusion and endothelial cell degeneration (1,2). These are followed by break down of blood retinal barrier (BRB) and leaky vasculature leading to hemorrhages, hard exudates, and retinal edema; structural changes involving the vascular wall leading to microaneurysms; and finally neovascularization, vitreous hemorrhage and fibrous tissue formation (3). Impaired vision due to macular edema, or vision loss due to neovascularization-induced vitreous hemorrhage or tractional retinal detachment usually takes place in the later stages of the disease.…”

Section: Introductionmentioning

confidence: 99%

Increase in acid sphingomyelinase level in human retinal endothelial cells and CD34+ circulating angiogenic cells isolated from diabetic individuals is associated with dysfunctional retinal vasculature and vascular repair process in diabetes

Kady

Yan

Salazar

et al. 2017

Journal of Clinical Lipidology

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Background Diabetic retinopathy (DR) is a microvascular disease that results from retinal vascular degeneration and defective repair due to diabetes induced endothelial progenitor dysfunction. Objective Understanding key molecular factors involved in vascular degeneration and repair is paramount for developing effective DR treatment strategies. We propose that diabetes-induced activation of acid sphingomyelinase (ASM) plays essential role in retinal endothelial and CD34+ circulating angiogenic cell (CAC) dysfunction in diabetes. Methods Human retinal endothelial cells (HRECs) isolated from control and diabetic donor tissue and human CD34+ CACs from control and diabetic patients were used in this study. ASM mRNA and protein expression was assessed by quantitative PCR and ELISA, respectively. To evaluate the effect of diabetes-induced ASM on HRECs and CD34+ CACs function, tube formation, CAC incorporation into endothelial tubes, and diurnal release of CD34+ CACs in diabetic individuals was determined. Results ASM expression level was significantly increased in HRECs isolated from diabetic compared to control donor tissue, as well as CD34+CACs and plasma of diabetic patients. A significant decrease in tube area was observed in HRECs from diabetic donors as compared to control HRECs. The tube formation deficiency was associated with increased expression of ASM in diabetic HRECs. Moreover, diabetic CD34+ CACs with high ASM showed defective incorporation into endothelial tubes. Diurnal release of CD34+ CACs was disrupted with the rhythmicity lost in diabetic patients. Conclusion Collectively, these findings support that diabetes-induced ASM upregulation has a marked detrimental effect on both retinal endothelial cells and CACs.

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