GPER-dependent estrogen signaling increases cardiac GCN5L1 expression and MCAD activity
Manning, J. R.; Thapa, D.; Zhang, M.; Stoner, M. W.; Sembrat, J. C.; Rojas, M.; Scott, I.
Show abstract
Reversible lysine acetylation regulates the activity of cardiac metabolic enzymes, including those controlling fuel substrate metabolism. Mitochondrial-targeted GCN5L1 and SIRT3 have been shown to regulate the acetylation status of mitochondrial enzymes, which results in alterations to the relative oxidation rates of fatty acids, glucose, and other fuels for contractile activity. However, the role that lysine acetylation plays in driving metabolic differences between male and female hearts is not currently known. In this study, we report that estrogens induce the expression of GCN5L1 via GPER agonism in cardiac cells, which increases the enzymatic activity and acetylation status of the fatty acid oxidation enzyme medium chain acyl-CoA dehydrogenase (MCAD).
Matching journals
The top 9 journals account for 50% of the predicted probability mass.
Similar papers in this journal
- Gestational arsenite exposure alters maternal postpartum heart size and induces Ca2+ handling dysregulation in cardiomyocytes 95%
- Adipocyte deletion of the RNA binding protein HuR induces cardiac hypertrophy and fibrosis 94%
- Relative contributions of correcting the diet and voluntary exercise to myocardial recovery in a two-hit murine model of heart failure with preserved ejection fraction. 93%
Similar papers in this journal
- Mitochondrial functional resilience after TFAM ablation in adult cardiomyocytes 93%
- Regulation of mitochondrial calcium uniporter expression and calcium signalling by lncRNA Tug1 in cardiomyocytes. 93%
- Breast cancer-associated skeletal muscle mitochondrial dysfunction and lipid accumulation is reversed by PPARG 92%
Similar papers in this journal
- Misoprostol Attenuates Cardiomyocyte Proliferation in the Neonatal Heart Through Bnip3 and Perinuclear Calcium Signaling 94%
- In vitro and in vivo roles of glucocorticoid and vitamin D receptors in the control of cardiomyocyte proliferative potential 94%
- Modulation of the Cardiac Sodium Channel Nav1.5 Peak and Late Currents by NAD+ Precursors 93%
Similar papers in this journal
Similar papers in this journal
- ERK3 Is Involved in Regulating Cardiac Fibroblast Function 93%
- Deletion of Sphingosine 1-Phosphate Receptor 1 in cardiomyocytes during development leads to abnormal ventricular conduction and fibrosis 93%
- Genetic Deletion of ASIC3 Alters Left Ventricular Remodeling and Autonomic Function After Myocardial Infarction in Mice 91%
"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.