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miR-214-3p 通过抑制 PTEN/AKT/mTOR 通路来减轻脓毒症诱导的小鼠心肌功能障碍。

miR-214-3p Attenuates Sepsis-Induced Myocardial Dysfunction in Mice by Inhibiting Autophagy through PTEN/AKT/mTOR Pathway.

机构信息

Emergency Department, The Third Hospital of Hebei Medical University, No. 139 Ziqiang Road, Qiaoxi Qu, Shijiazhuang City 050051, China.

Emergency Department, Cangzhou Central Hospital, No. 16 Xinhua Road, Yunhe Qu, Cangzhou City 061001, China.

出版信息

Biomed Res Int. 2020 Jul 2;2020:1409038. doi: 10.1155/2020/1409038. eCollection 2020.

DOI:10.1155/2020/1409038
PMID:32714974
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7359738/
Abstract

. More than half of the patients with sepsis would develop cardiac dysfunction, which is termed as sepsis-induced myocardial dysfunction (SIMD). Previous studies suggest that autophagy may play an important role in SIMD. The present study investigated whether miR-214-3p could attenuate SIMD by inhibiting autophagy. . In this article, we investigated the role of autophagy in a mouse model of cecal ligation and puncture (CLP). The structure and function of hearts harvested from the mice were evaluated. Myocardial autophagy levels were detected with immunohistochemical, immunofluorescent, and Western blot. . miR-214-3p can alleviate SIMD in septic mice by inhibiting the level of cardiac autophagy to attenuate myocardial dysfunction. Moreover, this study showed that miR-214-3p inhibited autophagy by silencing PTEN expression in the myocardial tissues of septic mice. . This study showed that miR-214-3p attenuated SIMD through myocardial autophagy inhibition by silencing PTEN expression and activating the AKT/mTOR pathway. The present findings supported that miR-214-3p may be a potential therapeutic target for SIMD.

摘要

. 超过一半的脓毒症患者会出现心功能障碍,这被称为脓毒症相关性心肌功能障碍(SIMD)。先前的研究表明,自噬可能在 SIMD 中发挥重要作用。本研究探讨了 miR-214-3p 是否可以通过抑制自噬来减轻 SIMD。. 在本文中,我们研究了自噬在盲肠结扎穿孔(CLP)小鼠模型中的作用。评估了从这些小鼠中提取的心脏的结构和功能。通过免疫组化、免疫荧光和 Western blot 检测心肌自噬水平。. miR-214-3p 通过抑制心脏自噬水平减轻脓毒症小鼠的 SIMD,从而减轻心肌功能障碍。此外,这项研究表明,miR-214-3p 通过沉默脓毒症小鼠心肌组织中的 PTEN 表达来抑制自噬。. 这项研究表明,miR-214-3p 通过沉默 PTEN 表达和激活 AKT/mTOR 通路来抑制心肌自噬,从而减轻 SIMD。这些发现表明,miR-214-3p 可能是 SIMD 的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c697/7359738/f0c775c6063a/BMRI2020-1409038.009.jpg
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