ArticleFrontiers in cell and developmental biology2022
Histone methyltransferase KMT2D contributes to the protection of myocardial ischemic injury.
Article in Frontiers in cell and developmental biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- YTH Domain Family 2 Promotes Tubal Factor Infertility through Reducing H3K4me1 Methylation of CYLD by KMT2D.Applied biochemistry and biotechnology · 2026Article
- Cardioprotective effect of acupuncture in mice with diabetic cardiomyopathy by alleviating cardiac fibrosis and apoptosis.American journal of cardiovascular disease · 2026Article
- Mechanisms of mitral valve development and disease.Frontiers in cardiovascular medicine · 2026Review
- Loss of Histone Methyltransferase KMT2D Attenuates Angiogenesis in the Ischemic Heart by Inhibiting the Transcriptional Activation of VEGF-A.Journal of cardiovascular translational research · 2023Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
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Abstract
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
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Registered trials
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