ArticleMolecular and cellular biology2011
Mouse cardiac acyl coenzyme a synthetase 1 deficiency impairs Fatty Acid oxidation and induces cardiac hypertrophy.
Article in Molecular and cellular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.
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Who cites it
114 citing papers in PubMed, 191 citations in OpenAlex.
- Genetic modifiers of response to glucose-insulin-potassium (GIK) infusion in acute coronary syndromes and associations with clinical outcomes in the IMMEDIATE trial.The pharmacogenomics journal · 2015Trial
- Article
- Metabolic Adaptation in Acute Ischemic Events: The Critical Role of Acyl-Coenzyme A Synthetase Family in Myocardial Infarction and Ischemic Stroke.Journal of the American Heart Association · 2026Review
- Low-Dose Cardiac Radiation Improves Electrical Function and Reduces Ventricular Arrhythmogenesis in Mice With Nonischemic Cardiomyopathy.JACC. Clinical electrophysiology · 2026Article
- Discovery of Sulfonamide Pantothenate Kinase Activators and Elucidation of the Role of Isoform Selectivity in Cellular Pantothenate Kinase Activation.Journal of medicinal chemistry · 2026Article
- Oxaliplatin-induced cardiotoxicity in mice is connected to the changes in energy metabolism in the heart tissue.Cardio-oncology (London, England) · 2026Article
- Acyl-CoA Synthetase 5 Knockout and Inhibitors Protect Against Diet-Induced Obesity in Mice by Activating the Ileal Brake.Journal of the Endocrine Society · 2026Article
- Semaglutide Reprograms Macrophages via the GLP-1R/PPARG/ACSL1 Pathway to Suppress Papillary Thyroid Carcinoma Growth.The Journal of clinical endocrinology and metabolism · 2025Article
- SOX2 drives esophageal squamous carcinoma by reprogramming lipid metabolism and histone acetylation landscape.Nature communications · 2025Article
- Moxibustion ameliorates abnormal subchondral bone remodeling by promoting ACSL1-mediated autophagy to degrade NLRP3 in osteoarthritis.Chinese medicine · 2025Article
- Plin5: A potential therapeutic target for type 2 diabetes mellitus.Diabetology & metabolic syndrome · 2025Article
- Metabolomic Panel for the Diagnosis of Heart Failure with Preserved Ejection Fraction.International journal of molecular sciences · 2025Article
- Evaluating the impact of lipids in isolated islet research.Frontiers in endocrinology · 2025Review
- Tissue specific roles of fatty acid oxidation.Advances in biological regulation · 2025Review
- Carnitine palmitoyltransferase 1 facilitates fatty acid oxidation in a non-cell-autonomous manner.Cell reports · 2024Article
- Plasma Proteomics of Type 2 Diabetes, Hypertension, and Co-Existing Diabetes/Hypertension in Thai Adults.Life (Basel, Switzerland) · 2024Article
- Characterization of ferroptosis-triggered pyroptotic signaling in heart failure.Signal transduction and targeted therapy · 2024Article
- Cardiac Metabolism, Reprogramming, and Diseases.Journal of cardiovascular translational research · 2024Review
- Maturation of lipid metabolism in the fetal and newborn sheep heart.American journal of physiology. Regulatory, integrative and comparative physiology · 2023Article
- Heterogeneous cardiac sympathetic innervation gradients promote arrhythmogenesis in murine dilated cardiomyopathy.JCI insight · 2023Article
54 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Long-chain acyl coenzyme A (acyl-CoA) synthetase isoform 1 (ACSL1) catalyzes the synthesis of acyl-CoA from long-chain fatty acids and contributes the majority of cardiac long-chain acyl-CoA synthetase activity. To understand its functional role in the heart, we studied mice lacking ACSL1 globally (Acsl1(T-/-)) and mice lacking ACSL1 in heart ventricles (Acsl1(H-/-)) at different times. Compared to littermate controls, heart ventricular ACSL activity in Acsl1(T-/-) mice was reduced more than 90%, acyl-CoA content was 65% lower, and long-chain acyl-carnitine content was 80 to 90% lower. The rate of [(14)C]palmitate oxidation in both heart homogenate and mitochondria was 90% lower than in the controls, and the maximal rates of [(14)C]pyruvate and [(14)C]glucose oxidation were each 20% higher. The mitochondrial area was 54% greater than in the controls with twice as much mitochondrial DNA, and the mRNA abundance of Pgc1α and Errα increased by 100% and 41%, respectively. Compared to the controls, Acsl1(T-/-) and Acsl1(H-/-) hearts were hypertrophied, and the phosphorylation of S6 kinase, a target of mammalian target of rapamycin (mTOR) kinase, increased 5-fold. Our data suggest that ACSL1 is required to synthesize the acyl-CoAs that are oxidized by the heart, and that without ACSL1, diminished fatty acid (FA) oxidation and compensatory catabolism of glucose and amino acids lead to mTOR activation and cardiac hypertrophy without lipid accumulation or immediate cardiac dysfunction.
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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.