Diabetic nephropathy (DN) is a serious microvascular complication of diabetes across the world. Recently, many circular RNAs (circRNAs) can exert a crucial role in DN progression. Our investigation was designed to study whether circ_0123996 was associated with DN and aimed to find out the underlying mechanisms. We observed that circ_0123996 expression was significantly increased in Type 2 diabetes (T2D) with DN in comparison to those patients without DN. Consistently, circ_0123996 was also obviously elevated in DN mice models and high glucose (HG)-incubated MMCs. Then, it was proved transfection of circ_0123996 siRNA in mice mesangial cells (MMCs) restrained MMCs proliferation greatly. In addition, it was demonstrated that decrease of circ_0123996 alleviated fibrosis-related protein expression including FN and Col-4 in MMCs. Next, it was confirmed by our study that circ_0123996 can serve as a sponge for miR-149-5p. miR-149-5p has been identified in several diseases including diabetes. At present, we observed that miR-149-5p was decreased in DN. Overexpression of miR-149-5p greatly repressed the effect of circ_0123996 on MMCs. BTB and CNC homology 1 (Bach1) is reported in various disease including some vascular diseases. Here, Bach1 was confirmed as a target of miR-149-5p. Circ_0123996 upregulated Bach1 expression and restrained MMCs proliferation and fibrosis through sponging miR-149-5p. Thus, it was revealed that circ_0123996 was involved in DN via sponging miR-149-5p and modulating Bach1 expression.

糖尿病肾病（DN）是世界范围内严重的糖尿病微血管并发症。最近，许多环状RNA（circRNA）可以在DN进程中发挥关键作用。我们的研究旨在研究circ_0123996是否与DN相关，并旨在找出潜在的机制。我们观察到，与没有DN的患者相比，在DN的2型糖尿病（T2D）中circ_0123996的表达显着增加。一致地，在DN小鼠模型和高葡萄糖（HG）孵育的MMC中，circ_0123996也明显升高。然后，证明在小鼠肾小球系膜细胞（MMCs）中转染circ_0123996 siRNA极大地抑制了MMCs的增殖。另外，已经证明，circ_0123996的减少减轻了MMC中纤维化相关蛋白的表达，包括FN和Col-4。下一个，我们的研究证实，circ_0123996可以用作miR-149-5p的海绵。已在包括糖尿病在内的多种疾病中鉴定出miR-149-5p。目前，我们观察到miR-149-5p的DN降低。miR-149-5p的过表达大大抑制了circ_0123996对MMC的作用。据报道，BTB和CNC同源性1（Bach1）存在多种疾病，包括某些血管疾病。在这里，Bach1被确认为miR-149-5p的靶标。Circ_0123996通过海绵miR-149-5p上调Bach1表达并抑制MMC增殖和纤维化。因此，揭示了circ_0123996通过海绵化miR-149-5p和调节Bach1表达而参与了DN。我们观察到miR-149-5p的DN降低。miR-149-5p的过表达大大抑制了circ_0123996对MMC的作用。据报道，BTB和CNC同源性1（Bach1）存在多种疾病，包括某些血管疾病。在这里，Bach1被确认为miR-149-5p的靶标。Circ_0123996通过海绵miR-149-5p上调Bach1表达并抑制MMC增殖和纤维化。因此，揭示了circ_0123996通过海绵化miR-149-5p和调节Bach1表达而参与了DN。我们观察到miR-149-5p的DN降低。miR-149-5p的过表达大大抑制了circ_0123996对MMC的作用。据报道，BTB和CNC同源性1（Bach1）存在多种疾病，包括某些血管疾病。在这里，Bach1被确认为miR-149-5p的靶标。Circ_0123996通过海绵miR-149-5p上调Bach1表达并抑制MMC增殖和纤维化。因此，揭示了circ_0123996通过海绵化miR-149-5p和调节Bach1表达而参与了DN。Circ_0123996通过海绵miR-149-5p上调Bach1表达并抑制MMC增殖和纤维化。因此，揭示了circ_0123996通过海绵化miR-149-5p和调节Bach1表达而参与了DN。Circ_0123996通过海绵miR-149-5p上调Bach1表达并抑制MMC增殖和纤维化。因此，揭示了circ_0123996通过海绵化miR-149-5p和调节Bach1表达而参与了DN。