Mettl13 protects against cardiac contractile dysfunction by negatively regulating C-Cbl-mediated ubiquitination of SERCA2a in ischemic heart failure

Yu, Shuting; Sun, ZhiYong; Wang, Xiuzhu; Ju, Tae-Jin; Wang, Changhao; Liu, Yingqi; Qu, Zhezhe; Liu, Kuiwu; Mei, Zhongting; Li, Na; Lu, Meixi; Wang, Fan; Huang, Min; Pang, Xiaochen; Jia, Yingqiong; Liu, Ying; Zhang, Yaozhi; Dou, Shi Xue; Jiang, Jiali; Li, Xin; Yang, Baofeng; Du, Weijie

doi:10.1007/s11427-022-2351-1

Sci. China Life Sci.

2023

DOI: 10.1007/s11427-022-2351-1

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Mettl13 protects against cardiac contractile dysfunction by negatively regulating C-Cbl-mediated ubiquitination of SERCA2a in ischemic heart failure

Shuting Yu

ZhiYong Sun

Xiuzhu Wang

et al.

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2024

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Cited by 6 publications

References 65 publications

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The m7G Methyltransferase Mettl1 Drives Cardiac Hypertrophy by Regulating SRSF9‐Mediated Splicing of NFATc4

Yu,

Sun,

et al. 2024

Advanced Science

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Cardiac hypertrophy is a key factor driving heart failure (HF), yet its pathogenesis remains incompletely elucidated. Mettl1‐catalyzed RNA N7‐methylguanosine (m7G) modification has been implicated in ischemic cardiac injury and fibrosis. This study aims to elucidate the role of Mettl1 and the mechanism underlying non‐ischemic cardiac hypertrophy and HF. It is found that Mettl1 is upregulated in human failing hearts and hypertrophic murine hearts following transverse aortic constriction (TAC) and Angiotensin II (Ang II) infusion. YY1 acts as a transcriptional factor for Mettl1 during cardiac hypertrophy. Mettl1 knockout alleviates cardiac hypertrophy and dysfunction upon pressure overload from TAC or Ang II stimulation. Conversely, cardiac‐specific overexpression of Mettl1 results in cardiac remodeling. Mechanically, Mettl1 increases SRSF9 expression by inducing m7G modification of SRSF9 mRNA, facilitating alternative splicing and stabilization of NFATc4, thereby promoting cardiac hypertrophy. Moreover, the knockdown of SRSF9 protects against TAC‐ or Mettl1‐induced cardiac hypertrophic phenotypes in vivo and in vitro. The study identifies Mettl1 as a crucial regulator of cardiac hypertrophy, providing a novel therapeutic target for HF.

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The m7G Methyltransferase Mettl1 Drives Cardiac Hypertrophy by Regulating SRSF9‐Mediated Splicing of NFATc4

Yu,

Sun,

et al. 2024

Advanced Science

Self Cite

View full text Add to dashboard Cite

show abstract

LncRNA CCRR maintains Ca2+ homeostasis against myocardial infarction through the FTO-SERCA2a pathway

Yang,

Xuan,

Wang

et al. 2024

Sci. China Life Sci.

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Calotropin attenuates ischemic heart failure after myocardial infarction by modulating SIRT1/FOXD3/SERCA2a pathway

Chen,

Yao,

Yao

et al. 2024

Biomedicine & Pharmacotherapy

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Mettl13 protects against cardiac contractile dysfunction by negatively regulating C-Cbl-mediated ubiquitination of SERCA2a in ischemic heart failure

Cited by 6 publications

References 65 publications

The m7G Methyltransferase Mettl1 Drives Cardiac Hypertrophy by Regulating SRSF9‐Mediated Splicing of NFATc4

The m7G Methyltransferase Mettl1 Drives Cardiac Hypertrophy by Regulating SRSF9‐Mediated Splicing of NFATc4

LncRNA CCRR maintains Ca2+ homeostasis against myocardial infarction through the FTO-SERCA2a pathway

Calotropin attenuates ischemic heart failure after myocardial infarction by modulating SIRT1/FOXD3/SERCA2a pathway

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