LncRNA-ZFAS1 Promotes Myocardial Ischemia-Reperfusion Injury Through DNA Methylation-Mediated Notch1 Down-Regulation in Mice

The most devastating and catastrophic deterioration of myocardial ischemia-reperfusion injury (MIRI) is cardiomyocyte death. Here we aimed to evaluate the role of lncRNA-ZFAS1 in MIRI and delineate its mechanism of action. The level of lncRNA-ZFAS1 was elevated in MIRI hearts, and artificial knockdo...

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Detalles Bibliográficos
Autores principales: Li, Mengmeng, Jiao, Lei, Shao, Yingchun, Li, Haodong, Sun, Lihua, Yu, Qi, Gong, Manyu, Liu, Dongping, Wang, Yanying, Xuan, Lina, Yang, Xuewen, Qu, Yunmeng, Wang, Yaqi, Jiang, Lintong, Han, Jingjing, Zhang, Ying, Zhang, Yong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2022
Materias:
Original Research - Preclinical
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9617129/
https://www.ncbi.nlm.nih.gov/pubmed/36317130
http://dx.doi.org/10.1016/j.jacbts.2022.06.004
Descripción
Sumario:The most devastating and catastrophic deterioration of myocardial ischemia-reperfusion injury (MIRI) is cardiomyocyte death. Here we aimed to evaluate the role of lncRNA-ZFAS1 in MIRI and delineate its mechanism of action. The level of lncRNA-ZFAS1 was elevated in MIRI hearts, and artificial knockdown of lncRNA-ZFAS1 in mice improved cardiac function. Notch1 is a potential target of lncRNA-ZFAS1, and lncRNA-ZFAS1 could bind to the promoter region of Notch1 and recruit DNMT3b to induce Notch1 methylation. Nicotinamide mononucleotide could promote the expression of Notch1 by competitively inhibiting the expression of DNMT3b and improving the apoptosis of cardiomyocytes and cardiac function.

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