Abstract

Diabetic retinopathy has recently been defined as a highly specific neurovascular complication of diabetes. The chronic progression of the impairment of the interdependence of neurovascular units (NVUs) is associated with the pathogenesis of diabetic retinopathy. The NVUs consist of neurons, glial cells, and vascular cells, and the interdependent relationships between these cells are disturbed under diabetic conditions. Clinicians should understand and update the current knowledge of the neurovascular impairments in diabetic retinopathy. Above all, neuronal cell death is an irreversible change, and it is directly related to vision loss in patients with diabetic retinopathy. Thus, neuroprotective and vasoprotective therapies for diabetic retinopathy must be established. Understanding the physiological and pathological interdependence of the NVUs is helpful in establishing neuroprotective and vasoprotective therapies for diabetic retinopathy. This review focuses on the pathogenesis of the neurovascular impairments and introduces possible neurovascular protective therapies for diabetic retinopathy.

Highlights

  • IntroductionAccording to the ninth edition of the International Diabetes Federation diabetes atlas, the estimated prevalence of diabetes will be 10.2% (578 million) by 2030 and 10.9%

  • According to the ninth edition of the International Diabetes Federation diabetes atlas, the estimated prevalence of diabetes will be 10.2% (578 million) by 2030 and 10.9%(700 million) by 2045 in the world [1]

  • The results of a recent study indicated that Long noncoding RNAs (LncRNAs) MALT1 facilitated its transcription by increasing the binding of the transcription factor at the Kelch-like ECH-associated protein 1 (Keap1) promoter, which results in preventing a translocation of the master regulator Nuclear factor erythroid 2-related factor 2 (Nrf2) and losing the antioxidant defense in diabetic retinopathy [120]

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Summary

Introduction

According to the ninth edition of the International Diabetes Federation diabetes atlas, the estimated prevalence of diabetes will be 10.2% (578 million) by 2030 and 10.9%. The Early Treatment Diabetic Retinopathy Study (ETDRS) has classified the stages of diabetic retinopathy based on vascular changes including dot/blot hemorrhages, hard/soft exudates, intraretinal microvascular abnormalities, and neovascularization [6]. Res. Public Health 2022, 19, 439 current treatment options for diabetic retinopathy and DME such as laser photocoagulation, intravitreal anti-vascular endothelial growth factor (VEGF) agent injections, or pars plana vitrectomy basically target the pathological changes based on the vascular abnormalities. The different cell types include neurons, glial cells, and vascular cells These cells constitute the NVUs, and the interdependence of these cells is associated with maintaining the homeostasis of the retinal environment under healthy conditions. This review focuses on the pathological changes of the NVUs and possible therapeutic options for neuroprotection and vasoprotection of diabetic retinopathy

Physiology of NVU in Normal Retina
Pathology of NVU in Diabetic Retinopathy
MyD88: myeloid differentiation primary response gene
Therapeutic Options for NVU Impairments in Diabetic Retinopathy
Antioxidants
Anti-Inflammatory Agents
Neurotrophic Factors and Others
Findings
Conclusions
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