miR‑214 ameliorates sepsis‑induced acute kidney injury via PTEN/AKT/mTOR‑regulated autophagy
- Zhenzhen Sang
- Shimin Dong
- Pu Zhang
- Yunxia Wei
Affiliations: Emergency Department, Cangzhou Central Hospital, Cangzhou, Hebei 061001, P.R. China, Department of Emergency, The Third Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, P.R. China
- Published online on: July 29, 2021 https://doi.org/10.3892/mmr.2021.12322
Copyright: © Sang
et al. This is an open access article distributed under the
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Commons Attribution License [CC BY_NC 4.0].
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Previous studies have suggested that oxidative stress and autophagy results in acute kidney injury (AKI) during sepsis and microRNA (miR)‑214 serves a vital role in the protection of kidneys subjected to oxidative stress. The present study aimed to test whether the renoprotection of miR‑214 is related to autophagy in sepsis. The role of autophagy was investigated in a mouse model of cecal ligation and puncture (CLP). Reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) was used to analyze the expression of miR‑214. The structure and function of kidneys harvested from the mice were evaluated. Kidney autophagy levels were detected with immunohistochemical, immunofluorescent and western blotting. It was found that miR‑214 could alleviate AKI in septic mice by inhibiting the level of kidney autophagy. Furthermore, miR‑214 inhibited autophagy by silencing PTEN expression in the kidney tissues of septic mice. These ﬁndings indicated that miR‑214 ameliorated CLP‑induced AKI by reducing oxidative stress and inhibiting autophagy through the regulation of the PTEN/AKT/mTOR pathway.