[Retracted] Antagonist targeting miR­106b­5p attenuates acute renal injury by regulating renal function, apoptosis and autophagy via the upregulation of TCF4.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the EdU staining assay data shown in Figs. 4C and 5C and the western blotting data shown in Fig. 4E were strikingly similar to data appearing in different form in other research articles written by different authors at different research institutes that had either already been published, or were submitted for publication at around the same time. Owing to the fact that contentious data in the above article had already been submitted for publication elsewhere prior to its submission to International Journal of Molecular Medicine, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Molecular Medicine 48: 169, 2021; DOI: 10.3892/ijmm.2021.5002].

Antagonist targeting miR­106b­5p attenuates acute renal injury by regulating renal function, apoptosis and autophagy via the upregulation of TCF4.

Acute renal injury (ARI) is a life­threatening condition and a main contributor to end­stage renal disease, which is mainly caused by ischemia­reperfusion (I/R). miR­106b­5p is a kidney function­related miRNA; however, whether miR­106b­5p regulates the progression of ARI remains unclear. The present study thus aimed to examine the effects of miR­106b­5p antagonist on the regulation of ARI progression. It was found that miR­106b­5p expression was upregulated in the renal tissue of rats with I/R­induced ARI and in NRK­52E rat renal proximal tubular epithelial cells subjected to hypoxia­reoxygenation (H/R). In vitro, H/R induction suppressed the proliferation, and promoted the apoptosis and autophagy of NRK­52E cells, whereas miR­106b­5p antagonist (inhibition of miR­106b­5p) promoted the proliferation, and attenuated the apoptosis and autophagy of NRK­52E cells under the H/R condition. Dual luciferase reporter gene assay validated that transcription factor 4 (TCF4) was a target of miR­106b­5p. It was further found that TCF4 overexpression promoted the proliferation, and inhibited the apoptosis and autophagy of NRK­52E cells subjected to H/R. Moreover, the effects of miR­106b­5p antagonist on NRK­52E cell proliferation, apoptosis and autophagy were mediated through the regulation of TCF4. In vivo, miR­106b­5p antagonist reduced the severity of renal injury, decreased cell proliferation in renal tissues and lowered the serum creatinine (Scr) and blood urea nitrogen (BUN) levels in the blood samples from rats with I/R­induced ARI. On the whole, the findings presented herein demonstrate that miR­106b­5p antagonist attenuates ARI by promoting the proliferation, and suppressing the apoptosis and autophagy of renal cells via upregulating TCF4.