ReviewCirculation research2014
Cardiac mitochondria and reactive oxygen species generation.
Review in Circulation research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 322 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
322 citing papers in PubMed, 1 synthesis or guideline pooled it, 589 citations in OpenAlex.
- Mapping current research and identifying hotspots of ferroptosis in cardiovascular diseases.Frontiers in cardiovascular medicine · 2022Pooled it
- Trial
- Cardiovascular-kidney-metabolic syndrome as a mitochondrial systems disorder.Nature reviews. Nephrology · 2026Review
- A Computational Model of Oxidative Stress in a Human Ventricular Myocyte.bioRxiv : the preprint server for biology · 2026Article
- Shifting the Balance: Mitochondrial Heteroplasmy as a Driver of Cardiac Disease.Circulation research · 2026Review
- Platelet membrane-fusing MSC-derived apoptotic extracellular vesicles enhanced cardiac repair after ischemia/reperfusion injury.Drug delivery and translational research · 2026Article
- Polystyrene Microplastics Induce Sustained Cardiovascular Redox Imbalance and Alter Mitochondrial Quality Control.Antioxidants (Basel, Switzerland) · 2026Article
- Review
- Piezo2-Initiated Ultrafast Signaling and Its Acquired Channelopathy in Light of Quantum Gravity Theory.International journal of molecular sciences · 2026Review
- Oxidative Stress-Induced Age-Related Bullous Keratopathy in Corneal Endothelial Cells With Lipid Droplets and Vacuoles.Investigative ophthalmology & visual science · 2026Article
- Review
- Natural products as multi‑target therapies for sepsis‑induced myocardial dysfunction (Review).International journal of molecular medicine · 2026Review
- Prussian blue nanoparticles targeting multiple PANoptosome-mediated PANoptosis for myocardial ischemia-reperfusion injury therapy.Nature communications · 2026Article
- The mechanism and clinical research of vagus nerve electrical stimulation in the treatment of myocardial ischemia-reperfusion injury.iScience · 2026Review
- BACH1-CHAC1-Glutathione Axis Aggravates Myocardial Ischemia-Reperfusion Injury by Enhancing Ferroptosis and Oxidative Stress.Antioxidants (Basel, Switzerland) · 2026Article
- Article
- Superoxide Mediates Radiation-Induced Cardiac Injury and Activates the Canonical Transforming Growth Factor-Beta Signaling Pathway.Journal of the American Heart Association · 2026Article
- Nanoparticle-Based Therapeutic Strategies for Pathological Cardiac Hypertrophy: Preclinical Advances, Translational Challenges, and Future Perspectives.International journal of nanomedicine · 2026Review
- Genomic Perspective on Heterogeneity of Organs and Body Aging.Aging cell · 2026Review
- Identifying sex-based disparities in porcine mitochondrial function.Animal biotechnology · 2025Article
262 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondrial reactive oxygen species (ROS) have emerged as an important mechanism of disease and redox signaling in the cardiovascular system. Under basal or pathological conditions, electron leakage for ROS production is primarily mediated by the electron transport chain and the proton motive force consisting of a membrane potential (ΔΨ) and a proton gradient (ΔpH). Several factors controlling ROS production in the mitochondria include flavin mononucleotide and flavin mononucleotide-binding domain of complex I, ubisemiquinone and quinone-binding domain of complex I, flavin adenine nucleotide-binding moiety and quinone-binding pocket of complex II, and unstable semiquinone mediated by the Q cycle of complex III. In mitochondrial complex I, specific cysteinyl redox domains modulate ROS production from the flavin mononucleotide moiety and iron-sulfur clusters. In the cardiovascular system, mitochondrial ROS have been linked to mediating the physiological effects of metabolic dilation and preconditioning-like mitochondrial ATP-sensitive potassium channel activation. Furthermore, oxidative post-translational modification by glutathione in complex I and complex II has been shown to affect enzymatic catalysis, protein-protein interactions, and enzyme-mediated ROS production. Conditions associated with oxidative or nitrosative stress, such as myocardial ischemia and reperfusion, increase mitochondrial ROS production via oxidative injury of complexes I and II and superoxide anion radical-induced hydroxyl radical production by aconitase. Further insight into cellular mechanisms by which specific redox post-translational modifications regulate ROS production in the mitochondria will enrich our understanding of redox signal transduction and identify new therapeutic targets for cardiovascular diseases in which oxidative stress perturbs normal redox signaling.
Indexed as
Identifiers
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.