ArticleThe Journal of biological chemistry2016
Type 2 Diabetes Dysregulates Glucose Metabolism in Cardiac Progenitor Cells.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
30 citing papers in PubMed, 44 citations in OpenAlex.
- Pyruvate kinase splice variants in fibroblasts influence cardiac remodeling after myocardial infarction in male mice.Journal of molecular and cellular cardiology · 2025Article
- PFKFB3 Connects Glycolytic Metabolism with Endothelial Dysfunction in Human and Rodent Obesity.Antioxidants (Basel, Switzerland) · 2025Article
- Phase partitioning of the neutrophil oxidative burst is coordinated by accessory pathways of glucose metabolism and mitochondrial activity.The Journal of biological chemistry · 2025Article
- Glutamine uptake and catabolism is required for myofibroblast formation and persistence.Journal of molecular and cellular cardiology · 2022Article
- Progressive stages of dysmetabolism are associated with impaired biological features of human cardiac stromal cells mediated by the oxidative state and autophagy.The Journal of pathology · 2022Article
- Single-cell transcriptomic profiling unveils dysregulation of cardiac progenitor cells and cardiomyocytes in a mouse model of maternal hyperglycemia.Communications biology · 2022Article
- Unraveling and Targeting Myocardial Regeneration Deficit in Diabetes.Antioxidants (Basel, Switzerland) · 2022Review
- Heart failure in diabetes.Metabolism: clinical and experimental · 2021Review
- Cell cycle induction in human cardiomyocytes is dependent on biosynthetic pathway activation.Redox biology · 2021Article
- Endothelial progenitor cells as critical mediators of environmental air pollution-induced cardiovascular toxicity.American journal of physiology. Heart and circulatory physiology · 2021Review
- Diabetes and Heart Failure: Multi-Omics Approaches.Frontiers in physiology · 2021Review
- Stable Isotopes for Tracing Cardiac Metabolism in Diseases.Frontiers in cardiovascular medicine · 2021Review
- Review
- Loss ofCancers · 2020Article
- Palbociclib treatment alters nucleotide biosynthesis and glutamine dependency in A549 cells.Cancer cell international · 2020Article
- Bioenergetics and translational metabolism: implications for genetics, physiology and precision medicine.Biological chemistry · 2019Review
- Mitochondrial calcium exchange links metabolism with the epigenome to control cellular differentiation.Nature communications · 2019Article
- Integration of flux measurements and pharmacological controls to optimize stable isotope-resolved metabolomics workflows and interpretation.Scientific reports · 2019Article
- Glucose Metabolism in Cardiac Hypertrophy and Heart Failure.Journal of the American Heart Association · 2019Review
- Effects of Rich-Polyphenols Extract of Dendrobium loddigesii on Anti-Diabetic, Anti-Inflammatory, Anti-Oxidant, and Gut Microbiota Modulation in db/db Mice.Molecules (Basel, Switzerland) · 2018Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
Abstract
Type 2 diabetes is associated with increased mortality and progression to heart failure. Recent studies suggest that diabetes also impairs reparative responses after cell therapy. In this study, we examined potential mechanisms by which diabetes affects cardiac progenitor cells (CPCs). CPCs isolated from the diabetic heart showed diminished proliferation, a propensity for cell death, and a pro-adipogenic phenotype. The diabetic CPCs were insulin-resistant, and they showed higher energetic reliance on glycolysis, which was associated with up-regulation of the pro-glycolytic enzyme 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (PFKFB3). In WT CPCs, expression of a mutant form of PFKFB, which mimics PFKFB3 activity and increases glycolytic rate, was sufficient to phenocopy the mitochondrial and proliferative deficiencies found in diabetic cells. Consistent with activation of phosphofructokinase in diabetic cells, stable isotope carbon tracing in diabetic CPCs showed dysregulation of the pentose phosphate and glycero(phospho)lipid synthesis pathways. We describe diabetes-induced dysregulation of carbon partitioning using stable isotope metabolomics-based coupling quotients, which relate relative flux values between metabolic pathways. These findings suggest that diabetes causes an imbalance in glucose carbon allocation by uncoupling biosynthetic pathway activity, which could diminish the efficacy of CPCs for myocardial repair.
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What OpenQuestion holds
Registered trials
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.