Aims: Diabetes nephropathy (DN) is one of the major complications in diabetes. With the improvement of people's living standards in China in recent years, the incidence of diabetes has become the main cause of end-stage renal disease. However, how and whether circ ASAP2 could mediate DN remain poorly understood. This study aimed to determine the function and its biological mechanism of circ ASAP2 on inflammation and ferroptosis of DN.
Methods: C57BL/6 mice were fed with a high-fat diet and injected with streptozotocin. Human renal glomerular endothelial cells stimulated with 20 mmol/L D-glucose.
Results: In mice model DN, circular ASAP2 expression level was down-regulated, and miR-770-5p expression level was up-regulated. Moreover, the inhibition of ASAP2 aggravated diabetic nephropathy in mice model. The inhibition of ASAP2 promoted inflammation and oxidative stress to aggravate renal injury in mice model. Circular ASAP2 was reducing inflammation and oxidative stress in vitro model. The inhibition of ASAP2 promoted ferroptosis in model of DN. CASAP2 suppressed miR-770-5p in DN. Additionally, miR-770-5p aggravated diabetic nephropathy in mice model. MiR-770-5p promoted inflammation and oxidative stress to aggravate renal injury in mice model. MiR-770-5p was increasing inflammation and oxidative stress in vitro model. Circular ASAP2 induced SLC7A11 expression in model of DN through SOX2 by miR-770-5p.
Conclusions: These results suggest that circ ASAP2 decreased inflammation and ferroptosis in DN through SOX2/SLC7A11 by miR-770-5p, which might serve as a target for improving the role of ferroptosis in DN.
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