Histone methyltransferase KMT2D contributes to the protection of myocardial ischemic injury.
glucocorticoid response element
ischemia
methyltransferase
serum
transcriptional regulation
Journal
Frontiers in cell and developmental biology
ISSN: 2296-634X
Titre abrégé: Front Cell Dev Biol
Pays: Switzerland
ID NLM: 101630250
Informations de publication
Date de publication:
2022
2022
Historique:
received:
17
05
2022
accepted:
30
06
2022
entrez:
8
8
2022
pubmed:
9
8
2022
medline:
9
8
2022
Statut:
epublish
Résumé
Histone H3 lysine 4 (H3K4) methyltransferase 2D (KMT2D) plays an important role in cell development in early life. However, the function of KMT2D in adult cells such as cardiomyocytes or neurons has not been reported. In this study, cardiomyocyte-specific KMT2D knockout (KMT2D-cKO) and control (KMT2D-Ctl) mice were exposed to sham or myocardial ischemia (MI) surgery. Depletion of KMT2D aggravated the ischemic area, led to the increased mortality (26.5% in KMT2D-cKO vs 12.5% in KMT2D-Ctl) of the mice, and weakened the left ventricular systolic function. RNA-seq analysis in cardiac tissues identified genes whose expression was changed by MI and KMT2D deletion. Combined with the genome-wide association study (GWAS) analysis, cardiac disease-associated genes
Identifiants
pubmed: 35938163
doi: 10.3389/fcell.2022.946484
pii: 946484
pmc: PMC9354747
doi:
Types de publication
Journal Article
Langues
eng
Pagination
946484Informations de copyright
Copyright © 2022 Liu, Meng, Li, Wang, Guo, Wang and Zhu.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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