Ophthalmic Disease in Diabetes

Henriques, José; Vaz-Pereira, Sara; Nascimento, João; Dutra-Medeiros, Marco; Henriques, Susana; Rosa, Paulo Caldeira

doi:10.1007/978-3-030-11815-0_49

Cited by 5 publications

(7 citation statements)

References 65 publications

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“…There was evidence revealed that Irf8 and Pu.1 could directly target each other's gene transcription and enhance the expression of microglial activation-related genes in neurodegenerative condi-tion. 30 However, in the retinal microglia of DR, the mechanism might be completely different and this needs further exploration for the more detailed mechanism.…”

Section: Discussionmentioning

confidence: 99%

Spleen Tyrosine Kinase Mediates Microglial Activation in Mice With Diabetic Retinopathy

Liu

Xu²,

Gao

2021

Trans. Vis. Sci. Tech.

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Diabetic retinopathy (DR) is a leading cause of blindness in developed countries, in which microglial activation is involved. However, the mechanism of microglial activation in DR remains largely unknown.Methods: We used Cx3cr1 CreERT2 ; Syk fl/fl mice to knockout microglial spleen tyrosine kinase (Syk) in the retina of mice (cKO mice) after streptozotocin injection to induce diabetes. We also isolated primary retinal microglia from wild-type and cKO mice, respectively, to explore the role of microglial Syk in DR. Results:The deletion of microglial Syk in the retina of mice or in the primary retinal microglia inhibited microglial activation and inflammatory response, eventually leading to the improvement of DR by regulating the expressions of interferon regulatory factor 8 (Irf8) and Pu.1 both in vivo and in vitro. Conclusions:The deletion of microglial Syk in the retina effectively ameliorated microglial activation-induced DR, suggesting the potential of microglial Syk as a therapeutic target for DR.Translational Relevance: Microglial spleen tyrosine kinase might serve as a potential therapeutic target for diabetic retinopathy.

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Section: Discussionmentioning

confidence: 99%

Spleen Tyrosine Kinase Mediates Microglial Activation in Mice With Diabetic Retinopathy

Liu

Xu²,

Gao

2021

Trans. Vis. Sci. Tech.

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“…Diabetic macular edema (DME) occurs when fluid accumulates on the retina, causing local swelling and distorted vision, ultimately resulting in permanent loss of vision. Diabetes-related vision loss can be averted in around 90% of instances, according to the Centres for Disease Control and Prevention (CDC) [4].…”

Section: Diabetic Macular Edemamentioning

confidence: 99%

“…Diabetes mellitus (DM) is a metabolic disorder caused by the lack of insulin production, insulin activity, or both. Further, chronic hyperglycemia is caused by insulin insufficiency, impairing carbohydrate, lipid, and protein metabolisms [3,4]. It is one of the leading global health issues that have arisen as a chronic non-communicable disease (CNCD).…”

Section: Introductionmentioning

confidence: 99%

“…It also sometimes leads to amputation of limbs, blindness, and vascular brain diseases [3]. Further, due to the occurrence of longterm hyperglycemia, the basement membrane of the eye accumulates enough toxic products, which cause irreversible damage to ophthalmic cells leading to cell death, ophthalmic opacity, and finally, vision impairment [4].…”

Section: Introductionmentioning

confidence: 99%

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Current Measures Against Ophthalmic Complications of Diabetes Mellitus-a Short Review

et al. 2021

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Diabetes mellitus (DM) is a metabolic disorder, whose prevalence is predicted to rise shortly. The present review focuses on the various ocular complications associated with DM, and the various ophthalmic formulation approaches developed to treat the same. Diabetic macular edema (DME), diabetic retinopathy, cataracts, and glaucoma are some of the major vision-threatening complications linked to DM. The ocular route of drug delivery has undergone several advancements in recent decades, the introduction of various novel drug delivery systems (DDS), various modifications in the existing formulation approaches, development of custom-designed personalized medications, being some of the major developments introduced in the field of ocular drug delivery. Due to the application of state-of-the-art technologies in the field of innovations related to ocular DDS, patients have been immensely benefited by the current modes of ocular treatment imparting fewer side effects, enhanced penetration, sustained drug effect, and so on. The present review includes and emphasizes the gradual development that has occurred from the conventional ophthalmic dosage forms to the currently reported novel ocular drug delivery approaches along with the related clinical research works.

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“…Diabetic retinopathy (DR) is a common microvascular complication of diabetes (Cheung et al, 2010;Henriques et al, 2015;Diallo et al, 2019). Early features of DR include blood-retina barrier (BRB) breakdown, capillary acellularity and pericyte loss and it has been confirmed that the main factor contributing to the progression of DR is chronic hyperglycemia (Stitt et al, 2016;Powers et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

MiR-124-3p Suppresses the Dysfunction of High Glucose-Stimulated Endothelial Cells by Targeting G3BP2

Zhao

2021

Front. Genet.

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Background: Diabetic retinopathy (DR) is the most important manifestation of diabetic microangiopathy. MicroRNAs (miRNAs), members of non-coding RNAs, have been frequently reported to regulate various diseases including DR. MiR-124-3p is involved in DR based on bioinformatics. The current study aimed to investigate the role of miR-124-3p in high glucose (HG)-treated human retinal microvascular endothelial cells (HRMECs), an in vitro model of DR.Methods: Bioinformatics analysis was applied to reveal the targets downstream miR-124-3p. A series of assays including CCK-8, luciferase reporter, western blot, and tube formation assays were used to explore the function and mechanism of miR-124-3p in HG-stimulated HRMECs.Results: We found out that miR-124-3p was downregulated in HG-stimulated HRMECs. Functionally, miR-124-3p overexpression restrained the HG-induced cell injury of HRMECs. Mechanistically, we predicted 5 potential target mRNAs of miR-124-3p. G3BP stress granule assembly factor 2 (G3BP2) was validated to bind with miR-124-3p. Rescue assays showed that miR-124-3p suppressed cell injury of HG-stimulated HRMECs through G3BP2. In addition, miR-124-3p regulated the p38MAPK signaling pathway by G3BP2, and G3BP2 promoted injury of HG-treated HRMECs through the activation of the p38MAPK signaling pathway.Conclusion: MiR-124-3p suppressed the dysfunctions of HG-treated HRMECs by targeting G3BP2 and activating the p38MAPK signaling. This new discovery provided a potential biomarker for DR treatment.

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Ophthalmic Disease in Diabetes

Cited by 5 publications

References 65 publications

Spleen Tyrosine Kinase Mediates Microglial Activation in Mice With Diabetic Retinopathy

Spleen Tyrosine Kinase Mediates Microglial Activation in Mice With Diabetic Retinopathy

Current Measures Against Ophthalmic Complications of Diabetes Mellitus-a Short Review

MiR-124-3p Suppresses the Dysfunction of High Glucose-Stimulated Endothelial Cells by Targeting G3BP2

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