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MetabolomicsDietary Glutamine Supplementation Mitigates Age-Associated Cardiac Decline by Restricting H3K27me3

Epigenetic alterations are central drivers of cardiovascular aging, with histone modifications regulating gene expression through chromatin remodeling and changes in DNA accessibility. However, the mechanisms underlying these epigenetic shifts in the aging heart remain poorly defined. Here, we id...

2026-02-11 | MTBLS13890 | MetaboLights
ProteomicsThe cardiac phospho-proteome during pressure overload in mice
Trans-aortic constriction (TAC) is a widely used murine model to study pressure overload-induced cardiac hypertrophy and heart failure. Despite its high prevalence during aortic stenosis or chronic arterial hypertension, the global alterations in cardiac proteome and phospho-proteome dynamics follow...
ORGANISM(S): Mus musculus (Mouse) 
2025-05-26 | PXD061784 | Pride
Heart failure Cardiac remodelling Signalling Tac Phosphorylation 
UnknownMicroRNA-27b-3p down-regulates FGF1 and aggravates pathological cardiac remodelling.
Not available
S-EPMC9302889 | biostudies-literature
GenomicsITIH5-mediated fibroblast/macrophage crosstalk exacerbates cardiac remodelling after myocardial infarction
ITIH5-mediated fibroblast/macrophage crosstalk exacerbates cardiac remodelling after myocardial infarction
PRJNA1140853 | ENA
TranscriptomicsA long noncoding RNA protects the heart from pathological hypertrophy
The role of long noncoding RNA (lncRNA) in adult hearts is unknown; also unclear is how lncRNA modulates nucleosome remodelling. An estimated 70% of mouse genes undergo antisense transcription1, including myosin heavy chain 7 (Myh7), which encodes molecular motor proteins for heart contraction2. Her...
ORGANISM(S): Homo sapiens 
2014-08-05 | E-GEOD-49716 | biostudies-arrayexpress
TranscriptomicsAnalysis of cardiac gene expression in response to isoproterenol-induced heart failure (part 1)
Myoglobin knockout mice (myo-/-) adapt to the loss of myoglobin by the activation of a variety of compensatory mechanisms on the structural and functional level. In order to analyze to what extent myo-/- mice would tolerate cardiac stress we used the model of chronic isoproterenol application to ind...
ORGANISM(S): Mus musculus 
2010-05-31 | E-GEOD-16243 | biostudies-arrayexpress
TranscriptomicsAnalysis of cardiac gene expression in response to isoproterenol-induced heart failure (part 2)
Myoglobin knockout mice (myo-/-) adapt to the loss of myoglobin by the activation of a variety of compensatory mechanisms on the structural and functional level. In order to analyze to what extent myo-/- mice would tolerate cardiac stress we used the model of chronic isoproterenol application to ind...
ORGANISM(S): Mus musculus 
2010-05-31 | E-GEOD-16246 | biostudies-arrayexpress
UnknownRespiratory chain signalling is essential for adaptive remodelling following cardiac ischaemia.
Not available
S-EPMC7131948 | biostudies-literature
GenomicsEndothelial deletion of the cytochrome P450 reductase leads to cardiac remodelling
Endothelial deletion of the cytochrome P450 reductase leads to cardiac remodelling
PRJNA887058 | ENA
ProteomicsCardiac Fibroblast Foxm1 Deficiency Prevents Pressure Overload-Induced Cardiac Remodeling via the Usp10/p38γ MAPK Axis
Aims: Cardiac fibroblasts (CFs) play a crucial role in cardiac remodelling, which is a common cause of heart failure (HF). However, the molecular mechanisms underlying the fibroblast-to-myofibroblast transition remain largely unknown. Foxm1 is well known in various cardiopulmonary pathologies. Howev...
ORGANISM(S): Mus musculus (Mouse) 
2024-03-10 | PXD050300 | Pride
Heart failure Cardiac remodelling Fibroblast Foxm1 
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