The m6A methylation enzyme METTL14 regulates myocardial ischemia/reperfusion injury through the Akt/mTOR signaling pathway

Wu, Chunchun; Chen, Youfang; Wang, Yaoguo; Xu, Chaoxiang; Cai, Yu; Zhang, Rongcheng; Peng, Fangzhan; Wang, Shengnan

doi:10.1007/s11010-023-04808-x

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2023

2025

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Cited by 5 publications

(1 citation statement)

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“…By regulating glycolysis and ferroptosis, KIAA1429 accelerates oral squamous cell carcinoma [ 27 ]. METTL14 regulates myocardial I/R injury via the Akt/mTOR signaling pathway [ 28 ].…”

Section: Introductionmentioning

confidence: 99%

KIAA1429 facilitates progression of hepatocellular carcinoma by modulating m6A levels in HPN

Meng,

Yang,

et al. 2023

Heliyon

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“…By regulating glycolysis and ferroptosis, KIAA1429 accelerates oral squamous cell carcinoma [ 27 ]. METTL14 regulates myocardial I/R injury via the Akt/mTOR signaling pathway [ 28 ].…”

Section: Introductionmentioning

confidence: 99%

KIAA1429 facilitates progression of hepatocellular carcinoma by modulating m6A levels in HPN

Meng,

Yang,

et al. 2023

Heliyon

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Mechanisms of METTL14‐Mediated m6A Modification in Promoting Iron Overload‐Induced Lipid Peroxidative Damage in Vascular Endothelial Cells to Aggravate Atherosclerosis

Min,

Lin,

Zhao

et al. 2024

J Biochem & Molecular Tox

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Atherosclerosis (AS) is a chronic multifactorial disease with damage to vascular endothelial cells (VECs). This study sought to delve into the mechanism of methyltransferase‐like 14 (METTL14) in iron overload‐induced lipid peroxidative damage in AS. AS mouse model and cell model were established. Levels of METTL14/circRNA coded by the Arhgap12 (circARHGAP12)/Aspartate β‐hydroxylase (ASPH) were determined. AS plaque area/lipid deposition/lipid metabolism in AS mice and iron overload in VECs were evaluated. N6‐methyladenosine (m6A) level and METTL14 enrichment and human antigen R (HuR) in circARHGAP12 or ASPH were measured. The mRNA stability of circARHGAP12 or ASPH was analyzed. We observed that METTL14 was upregulated in AS mice. METTL14 downregulation reduced plaque area/lipid deposition/iron overload/peroxidative damage in AS mice. In cell models, METTL14 downregulation could VEC injury/iron overload/lipid peroxidative damage. Mechanically, METTL14 increased the stability and expression of circARHGAP12 through m6A modification, further stabilized ASPH mRNA, and promoted ASPH transcription by binding to HuR. Overexpression of circARHGAP12 or inhibition of ASPH averted the protective role of METTL14 downregulation against iron overload‐induced peroxidative damage in AS. In conclusion, METTL14‐mediated m6A modification upregulated circARHGAP12 and ASPH to aggravate overload‐induced lipid peroxidative damage and facilitate AS progression.

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Aerobic exercise training attenuates ischemia-reperfusion injury in mice by decreasing the methylation level of METTL3-associated m6A RNA in cardiomyocytes

Zhang,

Huang,

Xuan

et al. 2025

Life Sciences

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The m6A methylation enzyme METTL14 regulates myocardial ischemia/reperfusion injury through the Akt/mTOR signaling pathway

Cited by 5 publications

References 34 publications

KIAA1429 facilitates progression of hepatocellular carcinoma by modulating m6A levels in HPN

KIAA1429 facilitates progression of hepatocellular carcinoma by modulating m6A levels in HPN

Mechanisms of METTL14‐Mediated m6A Modification in Promoting Iron Overload‐Induced Lipid Peroxidative Damage in Vascular Endothelial Cells to Aggravate Atherosclerosis

Aerobic exercise training attenuates ischemia-reperfusion injury in mice by decreasing the methylation level of METTL3-associated m6A RNA in cardiomyocytes

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