Region‐specific ischemia, neovascularization and macular oedema in treatment‐naïve proliferative diabetic retinopathy

Lange, Jason; Hadziahmetovic, Majda; Zhang, Jingfa; Li, Weiye

doi:10.1111/ceo.13168

Cited by 28 publications

(26 citation statements)

References 34 publications

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“…10 In our previous study, a strong correlation was found between central subfield thickness (CSFT) and the thickness of inner nuclear layer (INLT) in more severe DME (CSFT > 275 μm), suggesting that intracellular edema, particularly Müller glial edema, contributes to DME formation. 11 Müller cells, as specific macroglia in the retina, regulate the homeostasis of ion and water mainly through inward rectifying potassium channel 4.1 (Kir4.1) and aquaporin 4 (AQP4). [12][13][14] Müller cells are also the main source of vascular endothelial growth factor (VEGF) apart from vascular endothelial cells.…”

Section: Introductionmentioning

confidence: 99%

Anti-VEGF therapy prevents Müller intracellular edema by decreasing VEGF-A in diabetic retinopathy

et al. 2021

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Background Although vascular endothelial growth factor A (VEGF-A) is known to play a key role in causing retinal edema, whether and how VEGF-A induces intracellular edema in the retina still remains unclear. Methods Sprague-Dawley rats were rendered diabetic with intraperitoneal injection of streptozotocin. Intravitreal injection of ranibizumab was performed 8 weeks after diabetes onset. rMC-1 cells (rat Müller cell line) were treated with glyoxal for 24 h with or without ranibizumab. The expression levels of inwardly rectifying K+ channel 4.1 (Kir4.1), aquaporin 4 (AQP4), Dystrophin 71 (Dp71), VEGF-A, glutamine synthetase (GS) and sodium-potassium-ATPase (Na+-K+-ATPase) were examined using Western blot. VEGF-A in the supernatant of the cell culture was detected with ELISA. The intracellular potassium and sodium levels were detected with specific indicators. Results Compared with normal control, protein expressions of Kir4.1 and AQP4 were down-regulated significantly in diabetic rat retinas, which were prevented by ranibizumab. The above changes were recapitulated in vitro. Similarly, the intracellular potassium level in glyoxal-treated rMC-1 cells was increased, while the intracellular sodium level and Na+-K+-ATPase protein level remained unchanged, compared with control. However, ranibizumab treatment decreased intracellular sodium, but not potassium. Conclusion Ranibizumab protected Müller cells from diabetic intracellular edema through the up-regulation of Kir4.1 and AQP4 by directly binding VEGF-A. It also caused a reduction in intracellular osmotic pressure.

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Section: Introductionmentioning

confidence: 99%

Anti-VEGF therapy prevents Müller intracellular edema by decreasing VEGF-A in diabetic retinopathy

et al. 2021

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“…Analysis by Spearman's rank correlation showed the severity of non-perfusion in the peripheral zone was associated with the prevalence of IRMAs in the posterior zone. Lange et al [23] found that far-peripheral NPI was signi cantly associated with mid-peripheral NV index (linear regression: Y = 0.103*X + 0.841, p = 0.007). These results indicate that the ischemia-induced vascular abnormalities usually occurs at the border between the perfusion and non-perfusion areas, in concordance with previous study [24].…”

Section: Discussionmentioning

confidence: 98%

Dynamic versus static ultra-widefield fluorescein angiography in eyes with diabetic retinopathy: a pilot prospective cross-sectional study

Shen¹,

Niu²,

Chen³

et al. 2021

Int J Ophthalmol

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AIM: To analyze differences in ultra-widefield fluorescein angiography (UWFA) findings between dynamic and static images of eyes with diabetic retinopathy (DR). METHODS: This cross-sectional study included 28 eyes of 28 patients with DR undergoing UWFA. A series of UWFA images acquired from each patient were converted into a time-lapse video and used as a dynamic image. A single, clear, arteriovenous phase image was chosen as a static image. Non-perfusion index (NPI) and its correlation with vascular abnormalities in different zones were compared between dynamic and static UWFA imaging. RESULTS: NPI appeared to increase from the center to the far-periphery in both groups. Dynamic NPI was lower in the total retinal area (0.26 vs 0.29, P=0.009) and far-periphery (0.33 vs 0.36, adjusted P=0.042), which was contrary to the static NPI. Far-peripheral NPI was associated with intraretinal microvascular abnormality in the posterior area in both groups. CONCLUSION: Time-lapse dynamic UWFA imaging is a useful modality to differentially diagnose hypofluorescence in the most peripheral region. This modality could provide a reliable method for NPI measurement.

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Section: Methodsmentioning

confidence: 99%

“…al evaluated ISI for treatment naïve early stage PDR and found an ISI of 12% at the posterior pole, increasing to 38% in the far periphery[16]. Lange found ISI increasing from 20.5% in the posterior retina to 27.2% in the far periphery in patients with PDR[22].In addition, higher levels of ischemia have been shown to be associated with more advanced diabetic retinopathy[18]. Silva demonstrated higher levels of ischemia associated with more severe retinopathy, which plateaued for proliferative diabetic retinopathy[18].…”

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confidence: 99%

Ischemic Index and Distribution of Retinal Capillary Non-perfusion in Neovascular Glaucoma: a Retrospective Study

DeBoer¹,

Wong²,

Ameri³

2021

Preprint

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Purpose: To evaluate the pattern of retinal ischemia in newly diagnosed neovascular glaucoma (NVG).Methods: This is a retrospective single-center cross-sectional study of patients seen at LAC+USC Medical Center from January 2015 to April 2020. Patients with newly diagnosed NVG and ultra-widefield fluorescein angiography (UWFA) without prior panretinal photocoagulation were included. A total of 11 eyes from 10 patients met inclusion criteria. Three zones centered on the fovea were defined: posterior pole (within 2 disc-fovea lengths), mid periphery (between 2 and 3 disc-fovea lengths), and far periphery (>3 disc-fovea lengths). Ischemic index was calculated in these zones using ImageJ software.Results: The etiology of NVG was from proliferative diabetic retinopathy (n=9) and central retinal vein occlusion (n=2). Patients were aged between 48-74 years old. Ischemic index was found to be 91% in the far periphery, 77% in the mid periphery, and 42% at the posterior pole. The total average ischemic index was 76%. There was a statistically significant difference between the far periphery and posterior pole and mid periphery and posterior pole.Conclusions: High levels of retinal ischemia were found with newly diagnosed NVG. The pattern of ischemia was more pronounced in the far periphery than posterior pole.

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Region‐specific ischemia, neovascularization and macular oedema in treatment‐naïve proliferative diabetic retinopathy

Cited by 28 publications

References 34 publications

Anti-VEGF therapy prevents Müller intracellular edema by decreasing VEGF-A in diabetic retinopathy

Anti-VEGF therapy prevents Müller intracellular edema by decreasing VEGF-A in diabetic retinopathy

Dynamic versus static ultra-widefield fluorescein angiography in eyes with diabetic retinopathy: a pilot prospective cross-sectional study

Ischemic Index and Distribution of Retinal Capillary Non-perfusion in Neovascular Glaucoma: a Retrospective Study

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