Myocyte-specific overexpressing HDAC4 promotes myocardial ischemia/reperfusion injury
نویسندگان
چکیده
منابع مشابه
Specific inhibition of HDAC4 in cardiac progenitor cells enhances myocardial repairs.
We have recently shown that in vivo inhibition of histone deacetylase (HDAC) stimulates endogenous myocardial regeneration in infarcted hearts (Zhang L et al. J Pharmacol Exp Ther 341: 285-293, 2012). Furthermore, our observation demonstrates that HDAC inhibition promotes cardiogenesis, which is associated with HDAC4 reduction. However, it remains unknown as to whether specific inhibition of HD...
متن کاملAttenuation of myocardial ischemia/reperfusion injury in mice with myocyte-specific overexpression of endothelial nitric oxide synthase.
OBJECTIVE The role of nitric oxide (NO) in myocardial ischemia/reperfusion injury remains controversial as both NO donors and NO synthase (NOS) inhibitors have shown to be protective. We generated transgenic (TG) mice that overexpress endothelial NOS (eNOS) exclusively in cardiac myocytes to determine the effects of high cardiac NO levels on ischemia/reperfusion injury and cellular Ca(2+) homeo...
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During muscle regeneration, the transcription factor Pax7 stimulates the differentiation of satellite cells (SCs) toward the muscle lineage but restricts adipogenesis. Here, we identify HDAC4 as a regulator of Pax7-dependent muscle regeneration. In HDAC4-deficient SCs, the expression of Pax7 and its target genes is reduced. We identify HDAC4-regulated Lix1 as a Pax7 target gene required for SC ...
متن کاملMyocyte shearing, myocardial sheets, and microtubules.
The cytoskeleton of cardiac myocytes is a complex network of many interacting protein filaments and associated proteins with multiple functions: it forms structures responsible for maintaining cell shape and contractile filament registration, structural integrity, internal transport and cell division, and scaffolding for several putative signaling cascades.1 The tight coupling between the extra...
متن کاملCardiac Myocyte Apoptosis and Myocardial Remodeling
Sympathetic nerve activity increases in the heart during cardiac failure. Here, we hypothesized that 1 integrins play a protective role in chronic -adrenergic receptor–stimulated cardiac myocyte apoptosis and heart failure. L-isoproterenol (iso; 400 g/kg per hour) was infused in a group of wild-type (WT) and 1 integrin heterozygous knockout (hKO) mice. Left ventricular structural and functional...
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ژورنال
عنوان ژورنال: Molecular Medicine
سال: 2018
ISSN: 1076-1551,1528-3658
DOI: 10.1186/s10020-018-0037-2