ArticleJournal of molecular and cellular cardiology2014
Cardiac dysfunction and peri-weaning mortality in malonyl-coenzyme A decarboxylase (MCD) knockout mice as a consequence of restricting substrate plasticity.
Article in Journal of molecular and cellular cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Loss of ATP-Dependent Citrate Lyase Drives Left Ventricular Dysfunction by Metabolic Remodeling.Circulation · 2026Article
- Malonyl-CoA Decarboxylase: A Spotlight on Brain Aspects.Brain sciences · 2026Review
- Targeting immunometabolic pathways with AZD1656 alleviates inflammation and metabolic dysfunction in type 2 diabetic cardiomyopathy.Nature cardiovascular research · 2026Article
- MCD enzyme deficiency drives early mortality and multiorgan metabolic disruption in Dahl salt-sensitive rats.iScience · 2026Article
- Metabolomics-constrained modelling reveals dominant oxidative metabolism in the Egyptian fruit bat myocardium.PloS one · 2026Article
- Bat power-metabolic profiling of the Egyptian fruit batbioRxiv : the preprint server for biology · 2025Article
- Molecular Targets and Small Molecules Modulating Acetyl Coenzyme A in Physiology and Diseases.ACS pharmacology & translational science · 2025Review
- The mitochondrial citrate carrier SLC25A1 regulates metabolic reprogramming and morphogenesis in the developing heart.Communications biology · 2024Article
- Allele-specific dysregulation of lipid and energy metabolism in early-stage hypertrophic cardiomyopathy.Journal of molecular and cellular cardiology plus · 2024Article
- Analysis of the role of glucose metabolism-related genes in dilated cardiomyopathy based on bioinformatics.Journal of thoracic disease · 2023Article
- Serum Metabolomics Reveals Distinct Profiles during Ischemia and Reperfusion in a Porcine Model of Myocardial Ischemia-Reperfusion.International journal of molecular sciences · 2022Article
- Disruption of the circadian clock component BMAL1 elicits an endocrine adaption impacting on insulin sensitivity and liver disease.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Impact of reduced uterine perfusion pressure model of preeclampsia on metabolism of placenta, maternal and fetal hearts.Scientific reports · 2022Article
- Intracellular sodium elevation reprograms cardiac metabolism.Nature communications · 2020Article
- Immunometabolic cross-talk in the inflamed heart.Cell stress · 2019Review
- Age-Dependent Decline in Cardiac Function in Guanidinoacetate-Frontiers in physiology · 2019Article
- Is there a causal link between intracellular Na elevation and metabolic remodelling in cardiac hypertrophy?Biochemical Society transactions · 2018Review
- Proteomic and metabolomic changes driven by elevating myocardial creatine suggest novel metabolic feedback mechanisms.Amino acids · 2016Article
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Authors and funding
11 authors at 3 institutions in 3 countries.
Funding
Abstract
unlabelledInhibition of malonyl-coenzyme A decarboxylase (MCD) shifts metabolism from fatty acid towards glucose oxidation, which has therapeutic potential for obesity and myocardial ischemic injury. However, ~40% of patients with MCD deficiency are diagnosed with cardiomyopathy during infancy.
aimTo clarify the link between MCD deficiency and cardiac dysfunction in early life and to determine the contributing systemic and cardiac metabolic perturbations. METHODS AND
resultsMCD knockout mice ((-/-)) exhibited non-Mendelian genotype ratios (31% fewer MCD(-/-)) with deaths clustered around weaning. Immediately prior to weaning (18days) MCD(-/-) mice had lower body weights, elevated body fat, hepatic steatosis and glycogen depletion compared to wild-type littermates. MCD(-/-) plasma was hyperketonemic, hyperlipidemic, had 60% lower lactate levels and markers of cellular damage were elevated. MCD(-/-) hearts exhibited hypertrophy, impaired ejection fraction and were energetically compromised (32% lower total adenine nucleotide pool). However differences between WT and MCD(-/-) converged with age, suggesting that, in surviving MCD(-/-) mice, early cardiac dysfunction resolves over time. These observations were corroborated by in silico modelling of cardiomyocyte metabolism, which indicated improvement of the MCD(-/-) metabolic phenotype and improved cardiac efficiency when switched from a high-fat diet (representative of suckling) to a standard post-weaning diet, independent of any developmental changes.
conclusionsMCD(-/-) mice consistently exhibited cardiac dysfunction and severe metabolic perturbations while on a high-fat, low carbohydrate diet of maternal milk and these gradually resolved post-weaning. This suggests that dysfunction is a common feature of MCD deficiency during early development, but that severity is dependent on composition of dietary substrates.
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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.