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- W3119256043 endingPage "100940" @default.
- W3119256043 startingPage "100940" @default.
- W3119256043 abstract "The prevalence of diabetes has been rising steadily in the past half-century, along with the burden of its associated complications, including diabetic retinopathy (DR). DR is currently the most common cause of vision loss in working-age adults in the United States. Historically, DR has been diagnosed and classified clinically based on what is visible by fundoscopy; that is vasculature alterations. However, recent technological advances have confirmed pathology of the neuroretina prior to any detectable vascular changes. These, coupled with molecular studies, and the positive impact of anti-inflammatory therapeutics in DR patients have highlighted the central involvement of the innate immune system. Reminiscent of the systemic impact of diabetes, immune dysregulation has become increasingly identified as a key element of the pathophysiology of DR by interfering with normal homeostatic systems. This review uses the growing body of literature across various model systems to demonstrate the clear involvement of all three pillars of the immune system: immune-competent cells, mediators, and the complement system. It also demonstrates how the relative contribution of each of these requires more extensive analysis, including in human tissues over the continuum of disease progression. Finally, although this review demonstrates how the complex interactions of the immune system pose many more questions than answers, the intimately connected nature of the three pillars of the immune system may also point to possible new targets to reverse or even halt reverse retinopathy." @default.
- W3119256043 created "2021-01-18" @default.
- W3119256043 creator A5056580448 @default.
- W3119256043 creator A5057842034 @default.
- W3119256043 creator A5071882270 @default.
- W3119256043 date "2021-09-01" @default.
- W3119256043 modified "2023-10-13" @default.
- W3119256043 title "The innate immune system in diabetic retinopathy" @default.
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