ArticleMetabolites2020
Enhancing Glycolysis Protects against Ischemia-Reperfusion Injury by Reducing ROS Production.
Article in Metabolites, 2020. 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 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.
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, 42 citations in OpenAlex.
- Roles of inflammation and metabolic dysfunction in cardiovascular diseases: molecular mechanisms and therapeutic targets.Molecular biomedicine · 2026Review
- Integrated metabolomic profiling reveals metabolomic responses by epicardial and myocardial stromal cells to ischemia.Metabolomics : Official journal of the Metabolomic Society · 2026Article
- Mechanism of FoxO1 in the Metabolic Shift of Fetal Rat Heart.Molecules (Basel, Switzerland) · 2026Article
- Urine Proteomics as a Source of Biological Information and Outcome Predictor in Living Kidney Transplantation.Molecular & cellular proteomics : MCP · 2026Article
- Transcriptional remodeling of cardiomyocytes and fibroblasts during post-myocardial infarction recovery.Scientific reports · 2026Article
- Extended Preservation of Heart Grafts: LYPS Solution Maintains Cardiac Function During 20-Hour Static Cold Storage.International journal of molecular sciences · 2025Article
- Glycolysis-Related Genes,Cardiology research · 2025Article
- Reprogramming of Mitochondrial and Cellular Energy Metabolism in Fibroblasts and Cardiomyocytes: Mechanisms and Therapeutic Strategies in Cardiac Fibrosis.Journal of cardiovascular translational research · 2025Review
- ENO1 Dysfunction-Mediated Glycolytic Attenuation Exacerbates Oxidative Stress-Induced Retinal Ganglion Cell Death via Altered ATP Synthesis Pathway.Investigative ophthalmology & visual science · 2025Article
- Lactylation: A Novel Epigenetic Regulator of Cellular Senescence.Aging and disease · 2025Review
- Aerobic exercise-induced HIF-1α upregulation in heart failure: exploring potential impacts on MCT1 and MPC1 regulation.Molecular medicine (Cambridge, Mass.) · 2024Article
- Crosstalk among Reactive Oxygen Species, Autophagy and Metabolism in Myocardial Ischemia and Reperfusion Stages.Aging and disease · 2024Review
- HSPA12A maintains aerobic glycolytic homeostasis and Histone3 lactylation in cardiomyocytes to attenuate myocardial ischemia/reperfusion injury.JCI insight · 2024Article
- Cardiac Metabolism, Reprogramming, and Diseases.Journal of cardiovascular translational research · 2024Review
- Upregulation of Hsp27 via further inhibition of histone H2A ubiquitination confers protection against myocardial ischemia/reperfusion injury by promoting glycolysis and enhancing mitochondrial function.Cell death discovery · 2023Article
- The role of glycolytic metabolic pathways in cardiovascular disease and potential therapeutic approaches.Basic research in cardiology · 2023Review
- Muscone ameliorates myocardial ischemia‒reperfusion injury by promoting myocardial glycolysis.Heliyon · 2023Article
- Glycolysis Aids in Human Lens Epithelial Cells' Adaptation to Hypoxia.Antioxidants (Basel, Switzerland) · 2023Article
- Negative energy balance hinders prosocial helping behavior.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Nicotinamide restores tissue NAD+ and improves survival in rodent models of cardiac arrest.PloS one · 2023Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
After myocardial ischemia-reperfusion, fatty acid oxidation shows fast recovery while glucose oxidation rates remain depressed. A metabolic shift aimed at increasing glucose oxidation has shown to be beneficial in models of myocardial ischemia-reperfusion. However, strategies aimed at increasing glucose consumption in the clinic have provided mixed results and have not yet reached routine clinical practice. A better understanding of the mechanisms underlying the protection afforded by increased glucose oxidation may facilitate the transfer to the clinic. The purpose of this study was to evaluate if the modulation of reactive oxygen species (ROS) was involved in the protection afforded by increased glucose oxidation. Firstly, we characterized an H9C2 cellular model in which the use of glucose or galactose as substrates can modulate glycolysis and oxidative phosphorylation pathways. In this model, there were no differences in morphology, cell number, or ATP and PCr levels. However, galactose-grown cells consumed more oxygen and had an increased Krebs cycle turnover, while cells grown in glucose had increased aerobic glycolysis rate as demonstrated by higher lactate and alanine production. Increased aerobic glycolysis was associated with reduced ROS levels and protected the cells against simulated ischemia-reperfusion injury. Furthermore, ROS scavenger N-acetyl cysteine (NAC) was able to reduce the amount of ROS and to prevent cell death. Lastly, cells grown in galactose showed higher activation of mTOR/Akt signaling pathways. In conclusion, our results provide evidence indicating that metabolic shift towards increased glycolysis reduces mitochondrial ROS production and prevents cell death during ischemia-reperfusion injury.
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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.