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Tytuł pozycji:

FTO overexpression inhibits apoptosis of hypoxia/reoxygenation-treated myocardial cells by regulating m6A modification of Mhrt.

Tytuł :
FTO overexpression inhibits apoptosis of hypoxia/reoxygenation-treated myocardial cells by regulating m6A modification of Mhrt.
Autorzy :
Shen W; Department of Cardiovascular, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, No.17 Lujiang Road, Hefei, 230001, China.
Li H; Department of Gerontology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230001, China.
Su H; Department of Cardiovascular, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, No.17 Lujiang Road, Hefei, 230001, China.
Chen K; Department of Cardiovascular, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, No.17 Lujiang Road, Hefei, 230001, China.
Yan J; Department of Cardiovascular, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, No.17 Lujiang Road, Hefei, 230001, China. .
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Źródło :
Molecular and cellular biochemistry [Mol Cell Biochem] 2021 May; Vol. 476 (5), pp. 2171-2179. Date of Electronic Publication: 2021 Feb 06.
Typ publikacji :
Journal Article
Język :
English
Imprint Name(s) :
Publication: New York : Springer
Original Publication: The Hague, Dr. W. Junk B. V. Publishers.
References :
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Grant Information :
2016080802D113 The special projects of development in local science and technology guided by the central government; 1808085MH281 Natural Science Foundation of Anhui Province; WK9110000046 New Medicine of University of Science and Technology of China
Contributed Indexing :
Keywords: Apoptosis; FTO; Heart failure; Mhrt; m6A modification
Entry Date(s) :
Date Created: 20210206 Latest Revision: 20210421
Update Code :
20210421
DOI :
10.1007/s11010-021-04069-6
PMID :
33548009
Czasopismo naukowe
Heart failure (HF) is the end stage of many cardiovascular diseases and seriously threatens people's health. This article aimed to explore the biological role of fat-mass and obesity-associated gene (FTO) in HF. We constructed HF mouse model by transverse aortic constriction or intraperitoneal injection of doxorubicin. Mouse myocardial cells were exposed to hypoxia/reoxygenation (H/R). FTO and Mhrt were downregulated in heart tissues of HF mice. HF mice exhibited an increase in the total levels of N 6 methyladenosine (m 6 A) and the m 6 A levels of Mhrt. Moreover, FTO overexpression caused an upregulation of Mhrt and reduced m 6 A modification of Mhrt in the H/R-treated myocardial cells. FTO upregulation repressed apoptosis of H/R-treated myocardial cells. FTO knockdown had the opposite results. Mhrt overexpression reduced apoptosis of H/R-treated myocardial cells. Moreover, the influence conferred by FTO upregulation was abolished by Mhrt knockdown. In conclusion, our data demonstrate that FTO overexpression inhibits apoptosis of hypoxia/reoxygenation-treated myocardial cells by regulating m6A modification of Mhrt. Thus, FTO may be a target gene for HF treatment.

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