ArticleBiochimica et biophysica acta2014
Deficiency of cardiac Acyl-CoA synthetase-1 induces diastolic dysfunction, but pathologic hypertrophy is reversed by rapamycin.
Article in Biochimica et biophysica acta, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 37 citations in OpenAlex.
- A myeloid-dormant metabolic transcriptome identifies a poor-prognosis subgroup in hyperdiploid multiple myeloma with targetable vulnerabilities.Blood cancer journal · 2026Article
- 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
- Comparative analysis of metabolic and functional cardiac alterations in diet- and genetically induced mouse models of cardiac dysfunction.The FEBS journal · 2026Article
- Integrated Genomic-Metabolomic Analysis for Tri-Categorical Classification of Type 2 Diabetes Status in the Korean Ansan-Ansung Cohort.International journal of molecular sciences · 2025Article
- Identification of a novel InDel locus within theArchives animal breeding · 2025Article
- Tissue specific roles of fatty acid oxidation.Advances in biological regulation · 2025Review
- Transcriptome and Metabolome Profiling Provide New Insights into Disuse Muscle Atrophy in Chicken: The Potential Role of Fast-Twitch Muscle Fibers.International journal of molecular sciences · 2024Article
- Effects of Natural and Synthetic Astaxanthin on Growth, Body Color, and Transcriptome and Metabolome Profiles in the Leopard Coralgrouper (Animals : an open access journal from MDPI · 2023Article
- Loss of long-chain acyl-CoA synthetase 1 promotes hepatocyte death in alcohol-induced steatohepatitis.Metabolism: clinical and experimental · 2023Article
- Transcript variants of long-chain acyl-CoA synthase 1 have distinct roles in sheep lipid metabolism.Frontiers in genetics · 2022Article
- Transcriptional analysis of microRNAs related to unsaturated fatty acid synthesis by interfering bovine adipocyte ACSL1 gene.Frontiers in genetics · 2022Article
- Octanoate is differentially metabolized in liver and muscle and fails to rescue cardiomyopathy in CPT2 deficiency.Journal of lipid research · 2021Article
- Turnover rate of coenzyme A in mouse brain and liver.PloS one · 2021Article
- Acyl-CoA synthetases as regulators of brain phospholipid acyl-chain diversity.Prostaglandins, leukotrienes, and essential fatty acids · 2020Review
- Effects of Long-Chain Fatty Acyl-CoA Synthetase 1 on Diglyceride Synthesis and Arachidonic Acid Metabolism in Sheep Adipocytes.International journal of molecular sciences · 2020Article
- Rapamycin persistently improves cardiac function in aged, male and female mice, even following cessation of treatment.Aging cell · 2020Article
- Modeling the Transition From Decompensated to Pathological Hypertrophy.Journal of the American Heart Association · 2018Article
- Loss of cardiac carnitine palmitoyltransferase 2 results in rapamycin-resistant, acetylation-independent hypertrophy.The Journal of biological chemistry · 2017Article
- Sex difference in cardiac metabolism in nonischemic heart failure: Insight for prognostic value of altered cardiac metabolism.Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology · 2017Article
- Fuel availability and fate in cardiac metabolism: A tale of two substrates.Biochimica et biophysica acta · 2016Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
In mice with temporally-induced cardiac-specific deficiency of acyl-CoA synthetase-1 (Acsl1(H-/-)), the heart is unable to oxidize long-chain fatty acids and relies primarily on glucose for energy. These metabolic changes result in the development of both a spontaneous cardiac hypertrophy and increased phosphorylated S6 kinase (S6K), a substrate of the mechanistic target of rapamycin, mTOR. Doppler echocardiography revealed evidence of significant diastolic dysfunction, indicated by a reduced E/A ratio and increased mean performance index, although the deceleration time and the expression of sarco/endoplasmic reticulum calcium ATPase and phospholamban showed no difference between genotypes. To determine the role of mTOR in the development of cardiac hypertrophy, we treated Acsl1(H-/-) mice with rapamycin. Six to eight week old Acsl1(H-/-) mice and their littermate controls were given i.p. tamoxifen to eliminate cardiac Acsl1, then concomitantly treated for 10weeks with i.p. rapamycin or vehicle alone. Rapamycin completely blocked the enhanced ventricular S6K phosphorylation and cardiac hypertrophy and attenuated the expression of hypertrophy-associated fetal genes, including α-skeletal actin and B-type natriuretic peptide. mTOR activation of the related Acsl3 gene, usually associated with pathologic hypertrophy, was also attenuated in the Acsl1(H-/-) hearts, indicating that alternative pathways of fatty acid activation did not compensate for the loss of Acsl1. Compared to controls, Acsl1(H-/-) hearts exhibited an 8-fold higher uptake of 2-deoxy[1-(14)C]glucose and a 35% lower uptake of the fatty acid analog 2-bromo[1-(14)C]palmitate. These data indicate that Acsl1-deficiency causes diastolic dysfunction and that mTOR activation is linked to the development of cardiac hypertrophy in Acsl1(H-/-) mice.
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