Abstract Diabetic nephropathy (DN) is one of the most common complications of diabetes mellitus. Increasing evidence suggests that microRNA-30c-5p (miR-30c-5p) participates in the pathogenesis of DN, but the mechanism has not been clearly understood. Therefore, this study aimed to investigate the biological role of miR-30c-5p in human DN progression in vitro. Compared with the controls, DN tissues and high glucose-induced HK-2 cells had significantly reduced miR-30c-5p levels, while ROCK2 expression was prominently elevated. Additionally, the miR-30c-5p mimic distinctly facilitated cell proliferation and blocked cell apoptosis and epithelial–mesenchymal transition (EMT). However, ROCK2 was a target gene of miR-30c-5p, and the effects of miR-30c-5p mimic on cell proliferation, apoptosis and EMT were reversed by ROCK2 upregulation in vitro. Furthermore, the pathogenesis of DN was regulated by the miR-30c-5p/ROCK2 axis via the PI3K/AKT pathway. MiR-30c-5p regulating cell proliferation, apoptosis and EMT through targeting ROCK2 via the PI3K/AKT pathway provides the novel potential target for clinical treatment of DN.

中文翻译：

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MiR-30c-5p/ROCK2 轴通过 PI3K/AKT 信号通路在 HG 诱导的 HK-2 细胞中调节细胞增殖、凋亡和 EMT

摘要 糖尿病肾病（DN）是糖尿病最常见的并发症之一。越来越多的证据表明 microRNA-30c-5p (miR-30c-5p) 参与了 DN 的发病机制，但其机制尚不清楚。因此，本研究旨在研究 miR-30c-5p 在体外人类 DN 进展中的生物学作用。与对照组相比，DN 组织和高糖诱导的 HK-2 细胞显着降低了 miR-30c-5p 水平，而 ROCK2 表达显着升高。此外，miR-30c-5p 模拟物明显促进细胞增殖并阻止细胞凋亡和上皮间质转化 (EMT)。然而，ROCK2 是 miR-30c-5p 的靶基因，在体外 ROCK2 上调可逆转 miR-30c-5p 模拟物对细胞增殖、凋亡和 EMT 的影响。此外，DN的发病机制受miR-30c-5p/ROCK2轴通过PI3K/AKT通路调控。MiR-30c-5p 通过 PI3K/AKT 通路靶向 ROCK2 调节细胞增殖、凋亡和 EMT，为临床治疗 DN 提供了新的潜在靶点。