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Cardiomyocytes apoptosis myocardial - Wiley Online Library

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Last Updated: 23 October 2021

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Methyltransferase‐like 3 (METTL3) attenuates cardiomyocyte apoptosis with myocardial ischemia‐reperfusion (I/R) injury through miR‐25‐3p and miR‐873‐5p

In this study, we showed that METTL3 was downregulated in mice I/R myocardial cells and hypoxic/re oxygenated cardiomyocytes, and upregulation of METTL3 attenuated I/R and H/R caused cell apoptosis. On top of that, we evaluated out that two miRNAs, consisting of miR‐25‐3p and miR‐873‐5p, were favorably managed by METTL3 in cardiomyocytes in a DGCR8‐dependent manner. Furthermore, both miR‐25‐3p and miR‐873‐5p were significantly downregulated by I/R and H/R treatments in mice cells and cardiomyocytes, and overexpression of the above two miRNAs were efficient to boost cell practicality in cardiomyocytes under H/R anxiety. Next, we showed that METTL3 suppressed H/R caused cell fatality through upregulating miR‐25‐3p and miR‐873‐5p. The possible downstream mechanisms were checked out, and we expectedly discovered that METTL3 activated the PI3K/Akt path in H/R dealt with cardiomyocytes with modulating miR‐25‐3p and miR‐873‐5p, and the PI3K/Akt path inhibitor abrogated the safety impacts of METTL3 overexpression in cardiomyocytes with H/R treatment.

Source link: https://onlinelibrary.wiley.com/doi/10.1002/cbin.11706

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions