ReviewPhysiology (Bethesda, Md.)2008
Ion transport and energetics during cell death and protection.
Review in Physiology (Bethesda, Md.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.
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
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 124 citations in OpenAlex.
- Transient Ischemic Attacks Preceding Ischemic Stroke and the Possible Preconditioning of the Human Brain: A Systematic Review and Meta-Analysis.Frontiers in neurology · 2021Pooled it
- Myocardial Ischemia-Reperfusion Injury: Molecular Mechanisms and Innovative Therapeutic Strategies.Reviews in cardiovascular medicine · 2026Review
- Demonstration of beat-to-beat, on-demand ATP synthesis in ventricular myocytes reveals sex-specific mitochondrial and cytosolic dynamics.The Journal of physiology · 2026Article
- Energetic microdomains and the vascular control of neuronal and muscle excitability: Toward a unified model.The Journal of physiology · 2026Review
- Ion channels and cardiac disease: mechanisms and functions of a disintegrin and metalloproteases and their substrates.Frontiers in cell and developmental biology · 2026Review
- Ursodeoxycholic acid as a potential cardioprotective agent: molecular mechanisms, experimental evidence, and clinical perspectives.Frontiers in pharmacology · 2026Review
- Loss of Snord116 protects cardiomyocyte kinetics during ischemic stress.Journal of molecular and cellular cardiology plus · 2025Article
- Inhibition of RIPK1 or RIPK3 kinase activity post ischemia-reperfusion reduces the development of chronic kidney injury.The Biochemical journal · 2025Article
- The Role of TPM3 in Protecting Cardiomyocyte from Hypoxia-Induced Injury via Cytoskeleton Stabilization.International journal of molecular sciences · 2024Article
- Fueling the heartbeat: Dynamic regulation of intracellular ATP during excitation-contraction coupling in ventricular myocytes.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Maintaining energy provision in the heart: the creatine kinase system in ischaemia-reperfusion injury and chronic heart failure.Clinical science (London, England : 1979) · 2024Review
- Effect of GLP-1 Receptor Agonist on Ischemia Reperfusion Injury in Rats with Metabolic Syndrome.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Editorial: Current proceedings in magnetocardiology-past, present, future.Frontiers in cardiovascular medicine · 2024Article
- Health position paper and redox perspectives on reactive oxygen species as signals and targets of cardioprotection.Redox biology · 2023Review
- The Impact of Transfer-Related Ischemia on Free Flap Metabolism and Electrolyte Homeostasis-A New In Vivo Experimental Approach in Pigs.Journal of clinical medicine · 2023Article
- Effects of Prolonged Serum Calcium Suppression during Extracorporeal Cardiopulmonary Resuscitation in Pigs.Biomedicines · 2023Article
- Peptide Sodium Channels Modulator Mu-Agatoxin-Aa1a Prevents Ischemia-Reperfusion Injury of Cells.Molecules (Basel, Switzerland) · 2023Article
- Dynamics of necroptosis in kidney ischemia-reperfusion injury.Frontiers in immunology · 2023Article
- Therapeutic Targets for Regulating Oxidative Damage Induced by Ischemia-Reperfusion Injury: A Study from a Pharmacological Perspective.Oxidative medicine and cellular longevity · 2022Review
- Mitochondrial DNA Release Contributes to Intestinal Ischemia/Reperfusion Injury.Frontiers in pharmacology · 2022Review
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 at 2 institutions in 1 country.
Funding
Abstract
During ischemia, ATP and phosphocreatine (PCr) decline, whereas intracellular hydrogen ion, intracellular sodium (Na(+)), calcium (Ca(2+)), and magnesium (Mg(2+)) concentrations all rise. If the ischemia is relatively short and there is little irreversible injury (cell death), PCr, pH, Na(+), Mg(2+), and Ca(2+) all recovery quickly on reperfusion. ATP recovery can take up to 24 h because of loss of adenine base from the cell and the need for de novo synthesis. There are correlative data showing that a sustained rise in Ca(2+) during ischemia and/or lack of recovery during reperfusion is associated with irreversible cell injury. Interventions that reduce the rise in Ca(2+) during ischemia and reperfusion have been shown to reduce cell death. Therefore, a better understanding of the mechanisms responsible for the rise in Ca(2+) during ischemia and early reperfusion could have important therapeutic implications. This review will discuss mechanisms involved in alterations in ions and high energy phosphate metabolites in perfused or intact heart during ischemia and reperfusion.
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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.