NF-κB 介导的 Circ_35953 通过靶向 miR-7219-5p/HOOK3 和 IGFBP7 轴诱导脓毒症 AKI。

The Circ_35953 induced by the NF-κB mediated the septic AKI via targeting miR-7219-5p/HOOK3 and IGFBP7 axis.

机构信息

Department of Emergency, Second Xiangya Hospital, Central South University, Changsha, Hunan, China.

Emergency Medicine and Difficult Diseases Institute, Second Xiangya Hospital, Central South University, Changsha, Hunan, China.

出版信息

J Cell Mol Med. 2023 May;27(9):1261-1276. doi: 10.1111/jcmm.17731. Epub 2023 Mar 28.

A few studies suggested that CircRNAs were involved in the development of septic AKI. However，the role and regulation mechanism of CircRNA_35953 in septic AKI remains unclear. Here, we found that Circ_35953 was induced by LPS via activation of NF-κB signal in BUMPT cells. Functionally, Circ_35953 mediated the LPS induced the apoptosis in BUMPT cells. Moreover, we demonstrated that Circ_35953 sponged miR-7219-5p to upregulate the expression of HOOK3 and IGFBP7. Finally, we verified that knock down of Circ_35953 alleviated the progression of CLP-induced AKI via targeting the miR-7219-5p/HOOK3 and IGFBP7 signal. Collectively, the data suggested that Circ_35953 /miR-7219-5p/HOOK3 and IGFBP7 axis mediated the septic AKI, which also revealed a potential mechanism of septic AKI.

一些研究表明 CircRNAs 参与了脓毒症 AKI 的发生发展。然而，CircRNA_35953 在脓毒症 AKI 中的作用和调控机制尚不清楚。在这里，我们发现 Circ_35953 可被 LPS 通过激活 BUMPT 细胞中的 NF-κB 信号诱导。功能上，Circ_35953 介导了 LPS 诱导的 BUMPT 细胞凋亡。此外，我们证明 Circ_35953 可以通过海绵吸附 miR-7219-5p 来上调 HOOK3 和 IGFBP7 的表达。最后，我们通过靶向 miR-7219-5p/HOOK3 和 IGFBP7 信号证实，Circ_35953 的敲低可减轻 CLP 诱导的 AKI 的进展。总之，这些数据表明 Circ_35953/miR-7219-5p/HOOK3 和 IGFBP7 轴介导了脓毒症 AKI，这也揭示了脓毒症 AKI 的潜在机制。