Downregulated MicroRNA-327 Attenuates Oxidative Stress-Mediated Myocardial Ischemia Reperfusion Injury Through Regulating the FGF10/Akt/Nrf2 Signaling Pathway.
Downregulated MicroRNA-327 Attenuates Oxidative Stress-Mediated Myocardial Ischemia Reperfusion Injury Through Regulating the FGF10/Akt/Nrf2 Signaling Pathway.
复制标题
下调 MicroRNA-327 通过调节 FGF10/Akt/Nrf2 信号通路减轻氧化应激介导的心肌缺血再灌注损伤。
DOI：
10.3389/fphar.2021.669146
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发表时间：
2021
影响因子：
5.6
通讯作者：
Yang J
中科院分区：
文献类型：
--
作者：
Zheng T;Yang J;Zhang J;Yang C;Fan Z;Li Q;Zhai Y;Liu H;Yang J
虽然miR-327如前所述对心肌细胞具有保护作用，但其可能的机制仍需进一步探讨。本研究旨在探讨miR-327在心肌缺血/再灌注损伤(MI/RI)过程中氧化应激的作用及其机制。采用大鼠MI/RI模型、缺氧/复氧(H/R)模型和叔丁基氢过氧化氢(TBHP)诱导的H9c2细胞模型，检测心肌细胞的氧化应激和损伤情况。在体外，miR-327的下调抑制了H/R和TBHP诱导的氧化应激，并抑制了细胞凋亡。同时，miR-327基因敲除后，成纤维细胞生长因子10(FGF10)表达增强，p-PI3K和p-Akt被激活，Nrf2易位。然而，miR-327的过度表达却产生了相反的效果。与体外实验结果一致，miR-327的下调抑制了ROS的产生和内源性细胞的凋亡，减轻了I/R损伤。总之，抑制miR-327可通过调节FGF10/Akt/Nrf2通路提高心肌细胞的抗氧化能力和存活能力。
Although miR-327 had a protective effect on cardiomyocytes as described previously, the potential mechanism still needs further exploration. The aim of this study was to investigate the role and mechanism of miR-327 on oxidative stress in myocardial ischemia/reperfusion injury (MI/RI) process. Oxidative stress and cardiomyocytes injury were detected in rat model of MI/RI, hypoxia/reoxygenation (H/R), and tert-butyl hydroperoxide (TBHP) model of H9c2 cells. In vitro, downregulation of miR-327 inhibited both H/R- and TBHP-induced oxidative stress, and suppressed apoptosis. Meanwhile, fibroblast growth factor 10(FGF10) was enhanced by miR-327 knocked down, followed by the activation of p-PI3K and p-Akt, and the translocation of Nrf2. However, miR-327 overexpression performed with opposite effects. Consistent with the results in vitro, downregulation of miR-327 attenuated reactive oxygen species (ROS) generation as well as intrinsic apoptosis, and alleviated I/R injury. In conclusion, inhibition of miR-327 improved antioxidative ability and myocardial cell survival via regulating the FGF10/Akt/Nrf2 pathway.
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影响因子：
16.6
作者：
Fischer C;Seki T;Lim S;Nakamura M;Andersson P;Yang Y;Honek J;Wang Y;Gao Y;Chen F;Samani NJ;Zhang J;Miyake M;Oyadomari S;Yasue A;Li X;Zhang Y;Liu Y;Cao Y
通讯作者：
Cao Y
线粒体 PKM2 通过稳定 Bcl2 来调节氧化应激诱导的细胞凋亡。
影响因子：
44.1
作者：
Liang J;Cao R;Wang X;Zhang Y;Wang P;Gao H;Li C;Yang F;Zeng R;Wei P;Li D;Li W;Yang W
通讯作者：
Yang W
DOI：
10.1016/j.bbrc.2010.04.117
发表时间：
2010-05-28
影响因子：
3.1
作者：
Chartoumpekis, Dionysios;Ziros, Panos G.;Habeos, Ioannis G.
通讯作者：
Habeos, Ioannis G.
影响因子：
4.6
作者：
Daniel Sanchez-Hernandez, Cesar;Aide Torres-Alarcon, Lucero;Peon, Alberto N.
通讯作者：
Peon, Alberto N.
锌通过在心肌细胞缺氧/复氧的情况下诱导线粒体自噬来防止线粒体超氧化物的产生
影响因子：
3.3
作者：
Bian, Xiyun;Teng, Tianming;Xu, Zhelong
通讯作者：
Xu, Zhelong