Chee-Ming Lee

Objectives: Previous studies have demonstrated that patients with diabetic retinopathy (DR) have a higher prevalence of risk factors known to be associated with cardiovascular disease (CVD). We hypothesized that patients with more severe DR could have a higher relative risk of CVD. Methods: To test this hypothesis, we used the National Health Insurance Research Database (NHIRD) to evaluate whether associations exist between DR and CVD. The data for this nationwide population-based retrospective cohort study were obtained from the NHIRD in Taiwan from 2001 to 2013. The assessed study outcome used was the incidence and other statistical analyses of CVD in patients with DR during a 13-year follow-up period. Results: Our findings obtained from 2001 to 2013 suggest that the incidence rates of CVD are 2.026 times that of diabetes mellitus (DM) without DR (95% C.I. = 1.876–2.187) and 2.75 times that of DM with DR (95% C.I. = 2.487–3.04) compared with the Non-DM group. Conclusion: The relative risk of CVD in DR was greater than that in the Non-DM group for both men and women. Targeted monitoring of DM, especially the co-existence of diabetic retinopathy, is of utmost importance in the clinical care of the DM population.

Oxidative damage of retinal pigment epithelium (RPE) cells plays an important role in the pathogenesis of blindness-related diseases, such as age-related macular degeneration (AMD). Quercetin, a bioactive flavonoid compound, has been shown to have a protective effect against oxidative stress-induced cell apoptosis and inflammation in RPE cells; however, the detailed mechanism underlying this protective effect is unclear. Therefore, the aim of this study was to investigate the regulatory mechanism of quercetin in a sodium iodate (NaIO₃)-induced retinal damage. The clinical features of the mice, the production of oxidative stress, and the activity of autophagy and mitochondrial biogenesis were examined. In the mouse model, NaIO₃ treatment caused changes in the retinal structure and reduced pupil constriction, and quercetin treatment reversed the oxidative stress-related pathology by decreasing the level of superoxide dismutase 2 (SOD2) while enhancing the serum levels of catalase and glutathione. The increased level of reactive oxygen species in the NaIO₃-treated ARPE19 cells was improved by treatment with quercetin, accompanied by a reduction in autophagy and mitochondrial biogenesis. Our findings indicated that the effects of quercetin on regulating the generation of mtROS were dependent on increased levels of deacetyl-SOD2 through the Nrf2-PGC-1α-Sirt1 signaling pathway. These results demonstrated that quercetin may have potential therapeutic efficacy for the treatment of AMD through the regulation of mtROS homeostasis.