ArticleCirculation research2012
Cardiac-specific deletion of acetyl CoA carboxylase 2 prevents metabolic remodeling during pressure-overload hypertrophy.
Article in Circulation research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 186 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
186 citing papers in PubMed, 275 citations in OpenAlex.
- Single nucleus RNA sequencing identifies PLXNA4 upregulation in end-stage arrhythmogenic right ventricular cardiomyopathy.iScience · 2026Article
- METTL7B attenuates pathological cardiac hypertrophy via m6A-associated regulation of HK3.Molecular and cellular biochemistry · 2026Article
- Making sense of cardiomyopathy caused by deletion of acetyl-CoA carboxylase 1 and 2. Reply.The Journal of clinical investigation · 2026Article
- Making sense of cardiomyopathy caused by deletion of acetyl-CoA carboxylase 1 and 2.The Journal of clinical investigation · 2026Article
- Loss of the mitochondrial SAM transporter reveals a lipoylation-dependent metabolic vulnerability in the postnatal heart.Science advances · 2026Article
- Proteogenomics of Hypertrophic Cardiomyopathy Reveals Subtype-Specific Therapy.Circulation research · 2026Observational
- A Deep Learning Framework for the Discovery of Natural-Product Candidate Binders of Acetyl-CoA Carboxylase 2 (ACC2) with Potential Relevance to Cardiometabolic Lipid Metabolism.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Lgr6Genes & diseases · 2026Review
- Unrestrained fatty acid oxidation triggers heart failure in mice via cardiolipin loss and mitochondrial dysfunction.The Journal of clinical investigation · 2026Article
- Lipid droplets beyond storage: Cellular metabolic modulator in the diabetic heart (Review).International journal of molecular medicine · 2026Review
- cTnIR193H restrictive cardiomyopathy mice satisfy high-energy metabolic demands through regulating glucose metabolism.Genes & diseases · 2026Article
- Distinct immunometabolic signatures of type 1 versus type 2 diabetes in a murine model of myocardial infarction.Cardiovascular diabetology · 2026Article
- Unrestrained fatty acid oxidation triggers heart failure in mice via cardiolipin loss and mitochondrial dysfunction.bioRxiv : the preprint server for biology · 2026Article
- Sarco/Endoplasmic Reticulum CaJournal of the American Heart Association · 2026Article
- Research progress on metabolic abnormalities in myocardial hypertrophy.Frontiers in cardiovascular medicine · 2026Review
- Genetic deletion or pharmacological inhibition of acetyl-CoA carboxylase 2 enhances fatty acid oxidation and improves cardiac function and survival in the murine ATGL knockout model of severe heart failure.Journal of molecular and cellular cardiology plus · 2025Article
- Deletion of PTP1B in cardiomyocytes alters cardiac metabolic signaling to protect against cardiomyopathy induced by a high-fat diet.Science signaling · 2025Article
- Aerobic Exercise Alleviates Cardiac Dysfunction Correlated with Lipidomics and Mitochondrial Quality Control.Antioxidants (Basel, Switzerland) · 2025Article
- Modulation of cardiac fatty acid or glucose oxidation to treat heart failure in preclinical models: a systematic review and meta-analysis.Communications medicine · 2025Article
- Leucine-Rich Repeat-Containing G Protein-Coupled Receptor 6 Ameliorates Pressure Overload-Induced Cardiac Hypertrophy by Regulating Cardiomyocyte Metabolic Reprogramming.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
126 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
rationaleDecreased fatty acid oxidation (FAO) with increased reliance on glucose are hallmarks of metabolic remodeling that occurs in pathological cardiac hypertrophy and is associated with decreased myocardial energetics and impaired cardiac function. To date, it has not been tested whether prevention of the metabolic switch that occurs during the development of cardiac hypertrophy has unequivocal benefits on cardiac function and energetics.
objectiveBecause malonyl CoA production via acetyl CoA carboxylase 2 (ACC2) inhibits the entry of long chain fatty acids into the mitochondria, we hypothesized that mice with a cardiac-specific deletion of ACC2 (ACC2H-/-) would maintain cardiac FAO and improve function and energetics during the development of pressure-overload hypertrophy. METHODS AND
resultsACC2 deletion led to a significant reduction in cardiac malonyl CoA levels. In isolated perfused heart experiments, left ventricular function and oxygen consumption were similar in ACC2H-/- mice despite an ≈60% increase in FAO compared with controls (CON). After 8 weeks of pressure overload via transverse aortic constriction (TAC), ACC2H-/- mice exhibited a substrate utilization profile similar to sham animals, whereas CON-TAC hearts had decreased FAO with increased glycolysis and anaplerosis. Myocardial energetics, assessed by 31P nuclear magnetic resonance spectroscopy, and cardiac function were maintained in ACC2H-/- after 8 weeks of TAC. Furthermore, ACC2H-/--TAC demonstrated an attenuation of cardiac hypertrophy with a significant reduction in fibrosis relative to CON-TAC.
conclusionsThese data suggest that reversion to the fetal metabolic profile in chronic pathological hypertrophy is associated with impaired myocardial function and energetics and maintenance of the inherent cardiac metabolic profile and mitochondrial oxidative capacity is a viable therapeutic strategy.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.