上皮-间质转换
基因敲除
纤维化
癌症研究
下调和上调
长非编码RNA
肾
细胞
医学
生物
病理
内科学
细胞培养
基因
遗传学
作者
Zhao Min,Nan Li,Cheng Wei,Qingyan Zhang,Chunming Jiang,Hengjin Wang
标识
DOI:10.1016/j.mrfmmm.2023.111817
摘要
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.
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