Correlation Engine 2.0
Clear Search sequence regions

Sizes of these terms reflect their relevance to your search.

Emerging studies have revealed the mechanism of microRNAs (miRNAs) in acute kidney injury (AKI). However, almost no research focuses on miR-183-3p in AKI. Therefore, this study is started to explore the potential role of miR-183-3p from the perspective of Sirtuin (SIRT1)/forkhead box O3a (FOXO3a)/p53 up-regulated modulator of apoptosis (PUMA) in AKI. AKI rat models were established. miR-183-3p, SIRT1, deacetylated FOXO3a and PUMA expression in AKI were detected. The targeting relationship between miR-183-3p and SIRT1 was tested. AKI modeled rats were injected with miR-183-3p- or SIRT1-related sequences to identify their effects on AKI. Rat renal tubular epithelial cells NRK-52E were transfected with miR-183-3p- or SIRT1-related sequences for further exploration of their roles in vitro. Decreased SIRT1 and deacetylated FOXO3a and increased miR-183-3p and PUMA were found in AKI. SIRT1 was targeted by miR-183-3p. Down-regulated miR-183-3p or up-regulated SIRT1 attenuated renal tissue damage and fibrosis, and suppressed renal tubular epithelial cell apoptosis in renal tissues of AKI rats. Down-regulated miR-183-3p or up-regulated SIRT1 promoted proliferation and impaired fibrosis and apoptosis of renal tubular epithelial cells. Our study provides evidence that down-regulated miR-183-3p or up-regulated SIRT1 attenuates AKI via PUMA inhibition induced by FOXO3a deacetylation. Thus, miR-183-3p and SIRT1 can be the candidates for therapy of AKI. Copyright © 2021 Elsevier Inc. All rights reserved.


Hunian Li, Ping Chou, Fang Du, Liang Sun, Jie Liu, Wei Wang. Depleting microRNA-183-3p improves renal tubulointerstitial fibrosis after acute kidney injury via SIRT1/PUMA/FOXO3a deacetylation. Life sciences. 2021 Mar 15;269:119017

Expand section icon Mesh Tags

Expand section icon Substances

PMID: 33450262

View Full Text