Department of Nephrology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, No.321, Zhongshan Road, Nanjing 210008, Jiangsu, PR China.
Department of Nephrology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, No.321, Zhongshan Road, Nanjing 210008, Jiangsu, PR China.
Mutat Res. 2023 Jan-Jun;826:111817. doi: 10.1016/j.mrfmmm.2023.111817. Epub 2023 Apr 23.
Results of previous studies suggested that renal fibrosis and epithelial-mesenchymal transition (EMT) plays an important role in the process of renal fibrosis, but the underlying mechanism remains unclear. Long coding RNA (lncRNA) CRNDE has emerged as potent regulators of EMT programs, therefore, in present work, we examined the roles of LncRNA CRNDE/miR-29a-3p axis in renal fibrosis and the underlying mechanism. We found that in both renal fibrosis animal and cell models, lncRNA CRNDE was dynamically upregulated in animal models or cells by the treatment of TGF-β. Furthermore, knockdown of CRNDE to rat significantly inhibited EMT, prevented renal fibrosis. Finally, CRNDE regulates renal fibrosis through suppression of miR-29a-3p expression. Together, our results demonstrated that CRNDE acted as a regulator of renal fibrosis via targeting miR-29a-3p. Our findings may provide a potential therapeutic target for the treatment of renal fibrosis.
先前的研究结果表明，肾纤维化和上皮间质转化（EMT）在肾纤维化过程中起着重要作用，但潜在机制尚不清楚。长链非编码 RNA（lncRNA）CRNDE 已成为 EMT 程序的有效调节因子，因此，在本工作中，我们研究了 LncRNA CRNDE/miR-29a-3p 轴在肾纤维化中的作用及其潜在机制。我们发现，在肾纤维化动物和细胞模型中，lncRNA CRNDE 在动物模型或细胞中均由 TGF-β处理动态上调。此外，用 CRNDE 敲低大鼠显著抑制 EMT，防止肾纤维化。最后，CRNDE 通过抑制 miR-29a-3p 的表达来调节肾纤维化。总之，我们的结果表明，CRNDE 通过靶向 miR-29a-3p 作为肾纤维化的调节剂。我们的发现可能为治疗肾纤维化提供了一个潜在的治疗靶点。
