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.
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。
