ReviewRedox biology2014
Mitochondrial reactive oxygen species: a double edged sword in ischemia/reperfusion vs preconditioning.
Review in Redox biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 358 papers, 3 of them syntheses 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
358 citing papers in PubMed, 3 syntheses or guidelines pooled it, 699 citations in OpenAlex.
- Acute Inflammatory Responses to Blood Flow Restriction Training: A Systematic Review.Sports medicine - open · 2025Pooled it
- Exploring Astragaloside IV in Ischemic Heart Disease: A Comprehensive Systematic Review and Meta-Analysis of Preclinical Cardiotoxicity Models.Journal of biochemical and molecular toxicology · 2025Pooled it
- Effects and Mechanisms of Fisetin against Ischemia-reperfusion Injuries: A Systematic Review.Current pharmaceutical biotechnology · 2024Pooled it
- Intercellular Mitochondrial Transfer in the Nervous System: Roles of Tunneling Nanotubes, Mitochondrial Extracellular Vesicles, and Neuroimmune Bioenergetic Interactions.Molecular neurobiology · 2026Review
- Heart Meets Brain: Insights into Neurocardiac Pathophysiology.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Review
- A human-derived Pseudorabies virus isolate induces Cav2.2-sensitive CaMicrobiology spectrum · 2026Article
- Differential transcriptomic and metabolomic landscape between human hearts donated after cardiac vs brain death.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2026Article
- Platelet membrane-fusing MSC-derived apoptotic extracellular vesicles enhanced cardiac repair after ischemia/reperfusion injury.Drug delivery and translational research · 2026Article
- Evaluation of the Molecular Docking of Potential Targets and the Time-Dependent Myocardial Effects of Omeprazole in Normotensive and Spontaneously Hypertensive Rats Subjected to Cardiac Ischemia and Reperfusion.International journal of molecular sciences · 2026Article
- Sophocarpine Alleviates Renal Ischemia-Reperfusion Injury by Mitigating Oxidative Stress and Mitochondrial Dysfunction via the SIRT1/PGC-1α Axis.Biomedicines · 2026Article
- The Role of the Pentose Phosphate Pathway in Cardiovascular Diseases.Cardiovascular drugs and therapy · 2026Review
- Fuzheng Jiedu Tongluo Granule Alleviates Cerebral Ischemia/reperfusion Injury-induced Inflammation By Inhibiting Drp1-mediated TXNIP/NLRP3 Pathway.Molecular neurobiology · 2026Article
- Identification of Mitochondrial Dysfunction Genes as Diagnostic Biomarkers for Ischemic Stroke by Integrated Bioinformatics Analysis and Machine Learning.Journal of molecular neuroscience : MN · 2026Article
- Tyrosine 48 Phosphorylation of CytochromeBiomolecules · 2026Article
- Brazilin attenuates kidney ischemia-reperfusion injury by regulating inflammation, oxidative stress, and mitochondrial dysfunction.Histology and histopathology · 2026Article
- Cerebral Ischemia-Reperfusion Injury: Unraveling the Mitophagy-Oxidative Stress Axis for Neuroprotective Strategies.International journal of molecular sciences · 2026Review
- Receptor-Mitochondria Crosstalk in the Kynurenine Metabolic Pathway: Integrating Metabolomics and Clinical Mass Spectrometry.Antioxidants (Basel, Switzerland) · 2026Review
- Review
- Special Issue "Advances in the Prevention and Treatment of Ischemic Diseases".International journal of molecular sciences · 2026Article
- Exploring the effects of moxibustion on pathological remodeling in rats with myocardial ischemia-reperfusion injury based on mitochondrial cardiolipin protection.Frontiers in pharmacology · 2026Article
298 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Reductions in the blood supply produce considerable injury if the duration of ischemia is prolonged. Paradoxically, restoration of perfusion to ischemic organs can exacerbate tissue damage and extend the size of an evolving infarct. Being highly metabolic organs, the heart and brain are particularly vulnerable to the deleterious effects of ischemia/reperfusion (I/R). While the pathogenetic mechanisms contributing to I/R-induced tissue injury and infarction are multifactorial, the relative importance of each contributing factor remains unclear. However, an emerging body of evidence indicates that the generation of reactive oxygen species (ROS) by mitochondria plays a critical role in damaging cellular components and initiating cell death. In this review, we summarize our current understanding of the mechanisms whereby mitochondrial ROS generation occurs in I/R and contributes to myocardial infarction and stroke. In addition, mitochondrial ROS have been shown to participate in preconditioning by several pharmacologic agents that target potassium channels (e.g., ATP-sensitive potassium (mKATP) channels or large conductance, calcium-activated potassium (mBKCa) channels) to activate cell survival programs that render tissues and organs more resistant to the deleterious effects of I/R. Finally, we review novel therapeutic approaches that selectively target mROS production to reduce postischemic tissue injury, which may prove efficacious in limiting myocardial dysfunction and infarction and abrogating neurocognitive deficits and neuronal cell death in stroke.
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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.