Introduction:
The aim of the present study was to investigate the roles of long noncoding RNA (lncRNA) MALAT1 in the development of sepsis-induced acute kidney injury (septic AKI) and the underlying mechanism.

Material and methods:
The levels of MALAT1 in the serum of the septic AKI patients and healthy subjects were compared, and the targeting relationship between MALAT1 and miR-23a-3p was analyzed. Moreover, the effects of MALAT1 and miR-23a-3p on the proliferation and apoptosis of LPS-treated HK-2 cells were analyzed. Finally, the roles of ERK signaling during this process were analyzed.

Results:
We found that MALAT1 was markedly increased in serum of the septic AKI patients and LPS-treated cells. In addition, overexpression of MALAT1 relieved the injury induced by LPS in RMCs. Moreover, miR-23-a-3p has been confirmed as a target of MALAT1. Meanwhile, we also found that MALAT1 siRNA can increase the proliferation and inhibit the apoptosis of LPS-treated HK-2 cells through activating ERK signaling, and knockdown of miR-23a-3p can partially block the anti-apoptotic effect of MALAT1 siRNA.

Conclusions:
We report that MALAT1 can regulate the proliferation and apoptosis of LPS-treated HK-2 cells via targeting miR-23a-3p through regulating ERK signaling, suggesting that the MALAT1/miR-23a-3p axis could serve as a potential therapeutic target for the treatment of septic AKI.