ReviewMolecular and cellular biochemistry1998
Glucose and glycogen utilisation in myocardial ischemia--changes in metabolism and consequences for the myocyte.
Review in Molecular and cellular biochemistry, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 109 citations in OpenAlex.
- Emerging therapy strategies for energy metabolism in acute myocardial infarction.Journal of translational medicine · 2025Review
- Molecular Mechanisms of Microvascular Obstruction and Dysfunction in Percutaneous Coronary Interventions: From Pathophysiology to Therapeutics-A Comprehensive Review.International journal of molecular sciences · 2025Review
- Extracellular vesicles derived from different tissues attenuate cardiac dysfunction in murine MI models.Biology direct · 2023Article
- LncRNA LncHrt preserves cardiac metabolic homeostasis and heart function by modulating the LKB1-AMPK signaling pathway.Basic research in cardiology · 2021Article
- H9c2 Cardiomyocytes under Hypoxic Stress: Biological Effects Mediated by Sentinel Downstream Targets.Oxidative medicine and cellular longevity · 2021Article
- Lactate and Myocardiac Energy Metabolism.Frontiers in physiology · 2021Review
- Cardiac metabolism as a driver and therapeutic target of myocardial infarction.Journal of cellular and molecular medicine · 2020Review
- The optimal model of reperfusion injuryThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2020Article
- GLP-1 Improves Diastolic Function and Survival in Heart Failure with Preserved Ejection Fraction.Journal of cardiovascular translational research · 2018Article
- Differential effects of AMP-activated protein kinase in isolated rat atria subjected to simulated ischemia-reperfusion depending on the energetic substrates available.Pflugers Archiv : European journal of physiology · 2018Article
- Asiatic acid protests against myocardial ischemia/reperfusion injury via modulation of glycometabolism in rat cardiomyocyte.Drug design, development and therapy · 2018Article
- Compound danshen dripping pills modulate the perturbed energy metabolism in a rat model of acute myocardial ischemia.Scientific reports · 2016Article
- Diabetic hyperglycemia attenuates sympathetic dysfunction and oxidative stress after myocardial infarction in rats.Cardiovascular diabetology · 2014Article
- Impact of conditioning hyperglycemic on myocardial infarction rats: Cardiac cell survival factors.World journal of cardiology · 2014Review
- Arg972 Insulin receptor substrate-1 is associated with decreased serum angiotensin-converting enzyme 2 levels in acute myocardial infarction patients: in vivo and in vitro evidence.Cardiovascular diabetology · 2013Article
- Age-related changes in cellular electrophysiology and calcium handling for atrial fibrillation.Journal of cellular and molecular medicine · 2013Article
- Trimetazidine demonstrated cardioprotective effects through mitochondrial pathway in a model of acute coronary ischemia.Naunyn-Schmiedeberg's archives of pharmacology · 2013Article
- Glycolytic inhibition causes spontaneous ventricular fibrillation in aged hearts.American journal of physiology. Heart and circulatory physiology · 2011Article
- Hyperglycemia can delay left ventricular dysfunction but not autonomic damage after myocardial infarction in rodents.Cardiovascular diabetology · 2011Article
- Cardiovascular molecular imaging: focus on clinical translation.Circulation · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Experimentally, enhanced glycolytic flux has been shown to confer many benefits to the ischemic heart, including maintenance of membrane activity, inhibition of contracture, reduced arrhythmias, and improved functional recovery. While at moderate low coronary flows, the benefits of glycolysis appear extensive, the controversy arises at very low flow rates, in the absence of flow; or when glycolytic substrate may be present in excess, such that high glucose concentrations with or without insulin overload the cell with deleterious metabolites. Under conditions of total global ischemia, glycogen is the only substrate for glycolytic flux. Glycogenolysis may only be protective until the accumulation of metabolites (lactate, H+, NADH, sugar phosphates and Pi ) outweighs the benefit of the ATP produced. The possible deleterious effects associated with increased glycolysis cannot be ignored, and may explain some of the controversial findings reported in the literature. However, an optimal balance between the rate of ATP production and rate of accumulation of metabolites (determined by the glycolytic flux rate and the rate of coronary washout), may ensure optimal recovery. In addition, the effects of glucose utilisation must be distinguished from those of glycogen, differences which may be explained by functional compartmentation within the cell.
Indexed as
Identifiers
9546626W1579436835What 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.