Progressive retinal neurodegeneration and microvascular change in diabetic retinopathy: longitudinal study using OCT angiography

Kim, Ki‐Young; Kim, Eung Suk; Kim, Do-Gyun; Yu, Seung-Young

doi:10.1007/s00592-019-01395-6

Cited by 64 publications

(48 citation statements)

References 43 publications

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“…This observation is in contrast to that reported by Kim et al 58 . The study found a strong positive correlation between loss of macular ganglion cells/IPL and vessel density in the SCP from baseline to 24 months.…”

Section: Discussioncontrasting

confidence: 97%

Microvascular impairment as a biomarker of diabetic retinopathy progression in the long-term follow up in type 1 diabetes

Scarinci

Picconi

Virgili

et al. 2020

Sci Rep

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This study aimed to explore differences in vascular and structural parameters using optical coherence tomography angiography in patients with type 1 diabetes (DM1) with mild signs of diabetic retinopathy (DR) over a two-year follow-up period. Parafoveal vessel density (PVD) and foveal avascular zone (FAZ) area were analyzed. The thickness of three predefined retinal slabs was measured, including the inner limiting membrane (ILM)–inner plexiform layer (IPL), IPL–inner nuclear layer (INL), and the IPL–outer nuclear layer (ONL). Twenty-two patients with DM1 and 21 controls were included. There was no significant difference in the FAZ area, perimeter and acircularity index between cohorts over time. Baseline superficial capillary plexus PVD was approximately 10% lower in patients with diabetes than in controls (p = 0.001), and was 12% lower at 2 years (p = 0.002). There was no difference in the annual linear trend between the groups (− 0.5% in diabetics vs. controls, p = 0.736). Baseline deep capillary plexus (DCP) PVD was slightly lower in diabetics than in controls (− 4.4%, p = 0.047) and the difference increased at 2 years (− 12.6%, p < 0.001). The annual linear trend was − 2.7% in diabetic patients compared to controls (p = 0.009). In addition, the PVD of the DCP and the intermediate capillary plexus (ICP) were evaluated separately. Regarding the DCP PVD, no statistically significant difference at any time points in diabetic patients compared to controls and no statistically significant difference in the linear trend was found (p > 0.1). Conversely, no difference was recorded for parafoveal ICP density at individual time points (p > 0.1), but a statistically significant difference in the linear trend over time in diabetic patients compared to controls was recoded (− 3.2% per year, p = 0.001). Despite the apparent intergroup differences at baseline in structural OCT parameters, the differences including ILM–IPL (p = 0.273), IPL–INL (p = 0.708), and IPL–ONL (p = 0.054) were modest and not statistically significant with time. Therefore, the microvascular change of the deeper vessels might be a robust biomarker to evaluate the clinical progression of DR in DM1.

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Section: Discussioncontrasting

confidence: 97%

Microvascular impairment as a biomarker of diabetic retinopathy progression in the long-term follow up in type 1 diabetes

Scarinci

Picconi

Virgili

et al. 2020

Sci Rep

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“…Complex regulators are inhibited during retinal pathologies and this increases vascular alterations, dysfunction and photoreceptor cell death (95,96). Indeed, there is clinical evidence that neuronal cell death in DR precedes vascular changes in the retina (97).…”

Section: Mediators Of Inflammation In Diabetic Retinopathymentioning

confidence: 99%

Microglia and Inflammatory Responses in Diabetic Retinopathy

2020

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Diabetic retinopathy is a vision-threatening disease affecting neurons and microvasculature of the retina. The development of this disease is associated with the action of inflammatory factors that are connected to the activation of microglial cells, the resident tissue macrophages of the CNS. In the quiescent state, microglial cells help maintain tissue homeostasis in the retina through phagocytosis and control of low-grade inflammation. However, prolonged tissue stress due to hyperglycemia primes microglia to become overly reactive with the concomitant production of pro-inflammatory cytokines and chemokines causing chronic inflammation. In this review, we provide evidence of microglial cell activation and pro-inflammatory molecules associated with the development and progression of diabetic retinopathy. We further highlight innovative animal models that can mimic the disease in humans and discuss strategies in modulating microglial-mediated inflammation as potential therapeutic approaches in managing the disease.

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“…Some of the recent clinical studies on DR reported an early neuronal loss in the retina prior to the onset of visible vascular changes (22,23). Further, many basic research investigations have shown the activation of innate immune cells, mainly the microglial population, at different stages of disease progression in animal and human DR retinal tissues (24,25).…”

Section: Introductionmentioning

confidence: 99%

A Systematic Investigation on Complement Pathway Activation in Diabetic Retinopathy

et al. 2020

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The complement system plays a crucial role in retinal homeostasis. While the proteomic analysis of ocular tissues in diabetic retinopathy (DR) has shown the deposition of complement proteins, their exact role in the pathogenesis of DR is yet unclear. We performed a detailed investigation of the role of the complement system by evaluating the levels of major complement proteins including C3, C1q, C4b, Complement Factor B (CFB), and Complement Factor H (CFH) and their activated fragments from both the classical and alternative pathways in vitreous humor and serum samples from proliferative DR (PDR) patients and controls. Further, the expressions of complements and several other key pro-and anti-angiogenic genes in the serum and vitreous humor were analyzed in the blood samples of PDR and non-PDR (NPDR) patients along with controls without diabetes. We also assessed the pro-inflammatory cytokines and matrix metalloproteinases in the vitreous humor samples. There was a significant increase in C3 and its activated fragment C3bα' (110 kDa) along with a corresponding upregulation of CFH in the vitreous of PDR patients, which confirmed the increased activation of the alternative complement pathway in PDR. Likewise, a significant upregulation of angiogenic genes and downregulation of anti-angiogenic genes was seen in PDR and NPDR cases. Increased MMP9 activity and upregulation of inflammatory markers IL8 and sPECAM with a downregulation of anti-inflammatory marker IL-10 in PDR vitreous indicated the possible involvement of microglia in DR pathogenesis. Further, a significantly high C3 deposition in the capillary wall along with thickening of basement membranes and co-localization of CFH expression with CD11b +ve activated microglial cells in diabetic retina suggested microglia as a source of CFH in diabetic retina. The increased CFH levels could be a feedback mechanism for arresting excessive complement activation in DR eyes. A gradual increase of CFH and CD11b expression in retina with early to late changes in epiretinal membranes of DR patients indicated a major role for the alternative complement pathway in disease progression.

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Progressive retinal neurodegeneration and microvascular change in diabetic retinopathy: longitudinal study using OCT angiography

Cited by 64 publications

References 43 publications

Microvascular impairment as a biomarker of diabetic retinopathy progression in the long-term follow up in type 1 diabetes

Microvascular impairment as a biomarker of diabetic retinopathy progression in the long-term follow up in type 1 diabetes

Microglia and Inflammatory Responses in Diabetic Retinopathy

A Systematic Investigation on Complement Pathway Activation in Diabetic Retinopathy

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