Abstract
Diabetic retinopathy (DR) is a significant cause of vision loss and a research subject that is constantly being explored for new mechanisms of damage and potential therapeutic options. There are many mechanisms and pathways that provide numerous options for therapeutic interventions to halt disease progression. The purpose of the present literature review is to explore both basic science research and clinical research for proposed mechanisms of damage in diabetic retinopathy to understand the role of triglyceride and cholesterol dysmetabolism in DR progression. This review delineates mechanisms of damage secondary to triglyceride and cholesterol dysmetabolism vs. mechanisms secondary to diabetes to add clarity to the pathogenesis behind each proposed mechanism. We then analyze mechanisms utilized by both triglyceride and cholesterol dysmetabolism and diabetes to elucidate the synergistic, additive, and common mechanisms of damage in diabetic retinopathy. Gathering this research adds clarity to the role dyslipidemia has in DR and an evaluation of the current peer-reviewed basic science and clinical evidence provides a basis to discern new potential therapeutic targets.
Highlights
Diabetic retinopathy (DR) is a significant complication of diabetes mellitus (DM) characterized by ischemic microvascular disease of the retina and retinal neurodegeneration, leading to vision loss [1]
The potential mechanisms for this damage include microvascular damage, disruption of neurovascular coupling, decreased apoA1 HDL and Muller cell dysfunction [27]. While this retinal dysfunction did not alter the visual acuity, this study suggests that the oxidative stress from hyperlipidemia may create conditions in the retina that amplify damage from diabetes
This study showed that use of TRPV4 agonist resulted in extensive degenerative damage and retinal remodeling
Summary
Diabetic retinopathy (DR) is a significant complication of diabetes mellitus (DM) characterized by ischemic microvascular disease of the retina and retinal neurodegeneration, leading to vision loss [1]. While basic science evidence clarifies the molecular pathways of damage utilized by dyslipidemia, the clinical studies confirm these results and provide a basis for discussion of therapeutic interventions.
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