https://www.selleckchem.com/products/d609.html
EGR1 restoration abrogated miR-23c overexpression role in HG-stimulated HRMCs. Notably, circ-GNB4 could target miR-23c and EGR1 was targeted by miR-23c, as confirmed by dual-luciferase reporter assay and RNA immunoprecipitation. Moreover, EGR1 expression was positively modulated by circ-GNB4 via miR-23c. Collectively, circ-GNB4 might be a novel mechanism of DN-induced HRMCs injury, and there was a circ-GNB4/miR-23c/EGR1 pathway underlying the proliferation, extracellular matrix accumulation, inflammation and oxidative stress. This study su
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