TNC Accelerates Hypoxia-Induced Cardiac Injury in a METTL3-Dependent Manner

Cardiac fibrosis and cardiomyocyte apoptosis are reparative processes after myocardial infarction (MI), which results in cardiac remodeling and heart failure at last. Tenascin-C (TNC) consists of four distinct domains, which is a large multimodular glycoprotein of the extracellular matrix. It is als...
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Autor*in:	Hao Cheng [verfasserIn] Linnan Li [verfasserIn] Junqiang Xue [verfasserIn] Jianying Ma [verfasserIn] Junbo Ge [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2023

Schlagwörter:	myocardial infarction TNC METTL3

Übergeordnetes Werk:	In: Genes - MDPI AG, 2010, 14(2023), 3, p 591
Übergeordnetes Werk:	volume:14 ; year:2023 ; number:3, p 591

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3390/genes14030591

Katalog-ID:	DOAJ087358980

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520			\|a Cardiac fibrosis and cardiomyocyte apoptosis are reparative processes after myocardial infarction (MI), which results in cardiac remodeling and heart failure at last. Tenascin-C (TNC) consists of four distinct domains, which is a large multimodular glycoprotein of the extracellular matrix. It is also a key regulator of proliferation and apoptosis in cardiomyocytes. As a significant m<sup<6</sup<A regulator, METTL3 binds m<sup<6</sup<A sites in mRNA to control its degradation, maturation, stabilization, and translation. Whether METTL3 regulates the occurrence and development of myocardial infarction through the m<sup<6</sup<A modification of TNC mRNA deserves our study. Here, we have demonstrated that overexpression of METTL3 aggravated cardiac dysfunction and cardiac fibrosis after 4 weeks after MI. Moreover, we also demonstrated that TNC resulted in cardiac fibrosis and cardiomyocyte apoptosis after MI. Mechanistically, METTL3 led to enhanced m<sup<6</sup<A levels of TNC mRNA and promoted TNC mRNA stability. Then, we mutated one m<sup<6</sup<A site “A” to “T”, and the binding ability of METTL3 was reduced. In conclusion, METTL3 is involved in cardiac fibrosis and cardiomyocyte apoptosis by increasing m<sup<6</sup<A levels of TNC mRNA and may be a promising target for the therapy of cardiac fibrosis after MI.
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spelling	10.3390/genes14030591 doi (DE-627)DOAJ087358980 (DE-599)DOAJbe017ab03e034dbeb6f7a8e7c6ef1c78 DE-627 ger DE-627 rakwb eng QH426-470 Hao Cheng verfasserin aut TNC Accelerates Hypoxia-Induced Cardiac Injury in a METTL3-Dependent Manner 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Cardiac fibrosis and cardiomyocyte apoptosis are reparative processes after myocardial infarction (MI), which results in cardiac remodeling and heart failure at last. Tenascin-C (TNC) consists of four distinct domains, which is a large multimodular glycoprotein of the extracellular matrix. It is also a key regulator of proliferation and apoptosis in cardiomyocytes. As a significant m<sup<6</sup<A regulator, METTL3 binds m<sup<6</sup<A sites in mRNA to control its degradation, maturation, stabilization, and translation. Whether METTL3 regulates the occurrence and development of myocardial infarction through the m<sup<6</sup<A modification of TNC mRNA deserves our study. Here, we have demonstrated that overexpression of METTL3 aggravated cardiac dysfunction and cardiac fibrosis after 4 weeks after MI. Moreover, we also demonstrated that TNC resulted in cardiac fibrosis and cardiomyocyte apoptosis after MI. Mechanistically, METTL3 led to enhanced m<sup<6</sup<A levels of TNC mRNA and promoted TNC mRNA stability. Then, we mutated one m<sup<6</sup<A site “A” to “T”, and the binding ability of METTL3 was reduced. In conclusion, METTL3 is involved in cardiac fibrosis and cardiomyocyte apoptosis by increasing m<sup<6</sup<A levels of TNC mRNA and may be a promising target for the therapy of cardiac fibrosis after MI. myocardial infarction TNC METTL3 Genetics Linnan Li verfasserin aut Junqiang Xue verfasserin aut Jianying Ma verfasserin aut Junbo Ge verfasserin aut In Genes MDPI AG, 2010 14(2023), 3, p 591 (DE-627)614096537 (DE-600)2527218-4 20734425 nnns volume:14 year:2023 number:3, p 591 https://doi.org/10.3390/genes14030591 kostenfrei https://doaj.org/article/be017ab03e034dbeb6f7a8e7c6ef1c78 kostenfrei https://www.mdpi.com/2073-4425/14/3/591 kostenfrei https://doaj.org/toc/2073-4425 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 14 2023 3, p 591
allfields_unstemmed	10.3390/genes14030591 doi (DE-627)DOAJ087358980 (DE-599)DOAJbe017ab03e034dbeb6f7a8e7c6ef1c78 DE-627 ger DE-627 rakwb eng QH426-470 Hao Cheng verfasserin aut TNC Accelerates Hypoxia-Induced Cardiac Injury in a METTL3-Dependent Manner 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Cardiac fibrosis and cardiomyocyte apoptosis are reparative processes after myocardial infarction (MI), which results in cardiac remodeling and heart failure at last. Tenascin-C (TNC) consists of four distinct domains, which is a large multimodular glycoprotein of the extracellular matrix. It is also a key regulator of proliferation and apoptosis in cardiomyocytes. As a significant m<sup<6</sup<A regulator, METTL3 binds m<sup<6</sup<A sites in mRNA to control its degradation, maturation, stabilization, and translation. Whether METTL3 regulates the occurrence and development of myocardial infarction through the m<sup<6</sup<A modification of TNC mRNA deserves our study. Here, we have demonstrated that overexpression of METTL3 aggravated cardiac dysfunction and cardiac fibrosis after 4 weeks after MI. Moreover, we also demonstrated that TNC resulted in cardiac fibrosis and cardiomyocyte apoptosis after MI. Mechanistically, METTL3 led to enhanced m<sup<6</sup<A levels of TNC mRNA and promoted TNC mRNA stability. Then, we mutated one m<sup<6</sup<A site “A” to “T”, and the binding ability of METTL3 was reduced. In conclusion, METTL3 is involved in cardiac fibrosis and cardiomyocyte apoptosis by increasing m<sup<6</sup<A levels of TNC mRNA and may be a promising target for the therapy of cardiac fibrosis after MI. myocardial infarction TNC METTL3 Genetics Linnan Li verfasserin aut Junqiang Xue verfasserin aut Jianying Ma verfasserin aut Junbo Ge verfasserin aut In Genes MDPI AG, 2010 14(2023), 3, p 591 (DE-627)614096537 (DE-600)2527218-4 20734425 nnns volume:14 year:2023 number:3, p 591 https://doi.org/10.3390/genes14030591 kostenfrei https://doaj.org/article/be017ab03e034dbeb6f7a8e7c6ef1c78 kostenfrei https://www.mdpi.com/2073-4425/14/3/591 kostenfrei https://doaj.org/toc/2073-4425 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 14 2023 3, p 591
allfieldsGer	10.3390/genes14030591 doi (DE-627)DOAJ087358980 (DE-599)DOAJbe017ab03e034dbeb6f7a8e7c6ef1c78 DE-627 ger DE-627 rakwb eng QH426-470 Hao Cheng verfasserin aut TNC Accelerates Hypoxia-Induced Cardiac Injury in a METTL3-Dependent Manner 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Cardiac fibrosis and cardiomyocyte apoptosis are reparative processes after myocardial infarction (MI), which results in cardiac remodeling and heart failure at last. Tenascin-C (TNC) consists of four distinct domains, which is a large multimodular glycoprotein of the extracellular matrix. It is also a key regulator of proliferation and apoptosis in cardiomyocytes. As a significant m<sup<6</sup<A regulator, METTL3 binds m<sup<6</sup<A sites in mRNA to control its degradation, maturation, stabilization, and translation. Whether METTL3 regulates the occurrence and development of myocardial infarction through the m<sup<6</sup<A modification of TNC mRNA deserves our study. Here, we have demonstrated that overexpression of METTL3 aggravated cardiac dysfunction and cardiac fibrosis after 4 weeks after MI. Moreover, we also demonstrated that TNC resulted in cardiac fibrosis and cardiomyocyte apoptosis after MI. Mechanistically, METTL3 led to enhanced m<sup<6</sup<A levels of TNC mRNA and promoted TNC mRNA stability. Then, we mutated one m<sup<6</sup<A site “A” to “T”, and the binding ability of METTL3 was reduced. In conclusion, METTL3 is involved in cardiac fibrosis and cardiomyocyte apoptosis by increasing m<sup<6</sup<A levels of TNC mRNA and may be a promising target for the therapy of cardiac fibrosis after MI. myocardial infarction TNC METTL3 Genetics Linnan Li verfasserin aut Junqiang Xue verfasserin aut Jianying Ma verfasserin aut Junbo Ge verfasserin aut In Genes MDPI AG, 2010 14(2023), 3, p 591 (DE-627)614096537 (DE-600)2527218-4 20734425 nnns volume:14 year:2023 number:3, p 591 https://doi.org/10.3390/genes14030591 kostenfrei https://doaj.org/article/be017ab03e034dbeb6f7a8e7c6ef1c78 kostenfrei https://www.mdpi.com/2073-4425/14/3/591 kostenfrei https://doaj.org/toc/2073-4425 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 14 2023 3, p 591
allfieldsSound	10.3390/genes14030591 doi (DE-627)DOAJ087358980 (DE-599)DOAJbe017ab03e034dbeb6f7a8e7c6ef1c78 DE-627 ger DE-627 rakwb eng QH426-470 Hao Cheng verfasserin aut TNC Accelerates Hypoxia-Induced Cardiac Injury in a METTL3-Dependent Manner 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Cardiac fibrosis and cardiomyocyte apoptosis are reparative processes after myocardial infarction (MI), which results in cardiac remodeling and heart failure at last. Tenascin-C (TNC) consists of four distinct domains, which is a large multimodular glycoprotein of the extracellular matrix. It is also a key regulator of proliferation and apoptosis in cardiomyocytes. As a significant m<sup<6</sup<A regulator, METTL3 binds m<sup<6</sup<A sites in mRNA to control its degradation, maturation, stabilization, and translation. Whether METTL3 regulates the occurrence and development of myocardial infarction through the m<sup<6</sup<A modification of TNC mRNA deserves our study. Here, we have demonstrated that overexpression of METTL3 aggravated cardiac dysfunction and cardiac fibrosis after 4 weeks after MI. Moreover, we also demonstrated that TNC resulted in cardiac fibrosis and cardiomyocyte apoptosis after MI. Mechanistically, METTL3 led to enhanced m<sup<6</sup<A levels of TNC mRNA and promoted TNC mRNA stability. Then, we mutated one m<sup<6</sup<A site “A” to “T”, and the binding ability of METTL3 was reduced. In conclusion, METTL3 is involved in cardiac fibrosis and cardiomyocyte apoptosis by increasing m<sup<6</sup<A levels of TNC mRNA and may be a promising target for the therapy of cardiac fibrosis after MI. myocardial infarction TNC METTL3 Genetics Linnan Li verfasserin aut Junqiang Xue verfasserin aut Jianying Ma verfasserin aut Junbo Ge verfasserin aut In Genes MDPI AG, 2010 14(2023), 3, p 591 (DE-627)614096537 (DE-600)2527218-4 20734425 nnns volume:14 year:2023 number:3, p 591 https://doi.org/10.3390/genes14030591 kostenfrei https://doaj.org/article/be017ab03e034dbeb6f7a8e7c6ef1c78 kostenfrei https://www.mdpi.com/2073-4425/14/3/591 kostenfrei https://doaj.org/toc/2073-4425 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 14 2023 3, p 591
language	English
source	In Genes 14(2023), 3, p 591 volume:14 year:2023 number:3, p 591
sourceStr	In Genes 14(2023), 3, p 591 volume:14 year:2023 number:3, p 591
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	myocardial infarction TNC METTL3 Genetics
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container_title	Genes
authorswithroles_txt_mv	Hao Cheng @@aut@@ Linnan Li @@aut@@ Junqiang Xue @@aut@@ Jianying Ma @@aut@@ Junbo Ge @@aut@@
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callnumber-first	Q - Science
author	Hao Cheng
spellingShingle	Hao Cheng misc QH426-470 misc myocardial infarction misc TNC misc METTL3 misc Genetics TNC Accelerates Hypoxia-Induced Cardiac Injury in a METTL3-Dependent Manner
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topic_title	QH426-470 TNC Accelerates Hypoxia-Induced Cardiac Injury in a METTL3-Dependent Manner myocardial infarction TNC METTL3
topic	misc QH426-470 misc myocardial infarction misc TNC misc METTL3 misc Genetics
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title	TNC Accelerates Hypoxia-Induced Cardiac Injury in a METTL3-Dependent Manner
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title_sort	tnc accelerates hypoxia-induced cardiac injury in a mettl3-dependent manner
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title_auth	TNC Accelerates Hypoxia-Induced Cardiac Injury in a METTL3-Dependent Manner
abstract	Cardiac fibrosis and cardiomyocyte apoptosis are reparative processes after myocardial infarction (MI), which results in cardiac remodeling and heart failure at last. Tenascin-C (TNC) consists of four distinct domains, which is a large multimodular glycoprotein of the extracellular matrix. It is also a key regulator of proliferation and apoptosis in cardiomyocytes. As a significant m<sup<6</sup<A regulator, METTL3 binds m<sup<6</sup<A sites in mRNA to control its degradation, maturation, stabilization, and translation. Whether METTL3 regulates the occurrence and development of myocardial infarction through the m<sup<6</sup<A modification of TNC mRNA deserves our study. Here, we have demonstrated that overexpression of METTL3 aggravated cardiac dysfunction and cardiac fibrosis after 4 weeks after MI. Moreover, we also demonstrated that TNC resulted in cardiac fibrosis and cardiomyocyte apoptosis after MI. Mechanistically, METTL3 led to enhanced m<sup<6</sup<A levels of TNC mRNA and promoted TNC mRNA stability. Then, we mutated one m<sup<6</sup<A site “A” to “T”, and the binding ability of METTL3 was reduced. In conclusion, METTL3 is involved in cardiac fibrosis and cardiomyocyte apoptosis by increasing m<sup<6</sup<A levels of TNC mRNA and may be a promising target for the therapy of cardiac fibrosis after MI.
abstractGer	Cardiac fibrosis and cardiomyocyte apoptosis are reparative processes after myocardial infarction (MI), which results in cardiac remodeling and heart failure at last. Tenascin-C (TNC) consists of four distinct domains, which is a large multimodular glycoprotein of the extracellular matrix. It is also a key regulator of proliferation and apoptosis in cardiomyocytes. As a significant m<sup<6</sup<A regulator, METTL3 binds m<sup<6</sup<A sites in mRNA to control its degradation, maturation, stabilization, and translation. Whether METTL3 regulates the occurrence and development of myocardial infarction through the m<sup<6</sup<A modification of TNC mRNA deserves our study. Here, we have demonstrated that overexpression of METTL3 aggravated cardiac dysfunction and cardiac fibrosis after 4 weeks after MI. Moreover, we also demonstrated that TNC resulted in cardiac fibrosis and cardiomyocyte apoptosis after MI. Mechanistically, METTL3 led to enhanced m<sup<6</sup<A levels of TNC mRNA and promoted TNC mRNA stability. Then, we mutated one m<sup<6</sup<A site “A” to “T”, and the binding ability of METTL3 was reduced. In conclusion, METTL3 is involved in cardiac fibrosis and cardiomyocyte apoptosis by increasing m<sup<6</sup<A levels of TNC mRNA and may be a promising target for the therapy of cardiac fibrosis after MI.
abstract_unstemmed	Cardiac fibrosis and cardiomyocyte apoptosis are reparative processes after myocardial infarction (MI), which results in cardiac remodeling and heart failure at last. Tenascin-C (TNC) consists of four distinct domains, which is a large multimodular glycoprotein of the extracellular matrix. It is also a key regulator of proliferation and apoptosis in cardiomyocytes. As a significant m<sup<6</sup<A regulator, METTL3 binds m<sup<6</sup<A sites in mRNA to control its degradation, maturation, stabilization, and translation. Whether METTL3 regulates the occurrence and development of myocardial infarction through the m<sup<6</sup<A modification of TNC mRNA deserves our study. Here, we have demonstrated that overexpression of METTL3 aggravated cardiac dysfunction and cardiac fibrosis after 4 weeks after MI. Moreover, we also demonstrated that TNC resulted in cardiac fibrosis and cardiomyocyte apoptosis after MI. Mechanistically, METTL3 led to enhanced m<sup<6</sup<A levels of TNC mRNA and promoted TNC mRNA stability. Then, we mutated one m<sup<6</sup<A site “A” to “T”, and the binding ability of METTL3 was reduced. In conclusion, METTL3 is involved in cardiac fibrosis and cardiomyocyte apoptosis by increasing m<sup<6</sup<A levels of TNC mRNA and may be a promising target for the therapy of cardiac fibrosis after MI.
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title_short	TNC Accelerates Hypoxia-Induced Cardiac Injury in a METTL3-Dependent Manner
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