ReviewAntioxidants (Basel, Switzerland)2022
Yin and Yang of NADPH Oxidases in Myocardial Ischemia-Reperfusion.
Review in Antioxidants (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 41 citations in OpenAlex.
- Review
- Spatiotemporal dynamics of reactive oxygen species: implications for cellular homeostasis and redox therapies.Cellular & molecular biology letters · 2026Review
- Redox Control in Platelet Activity and Therapy.Antioxidants (Basel, Switzerland) · 2025Review
- Roles of Autophagy and Oxidative Stress in Cardiovascular Disease.Antioxidants (Basel, Switzerland) · 2025Review
- p22Nature cardiovascular research · 2025Article
- The Redox Revolution in Brain Medicine: Targeting Oxidative Stress with AI, Multi-Omics and Mitochondrial Therapies for the Precision Eradication of Neurodegeneration.International journal of molecular sciences · 2025Review
- Management of ROS and Regulatory Cell Death in Myocardial Ischemia-Reperfusion Injury.Molecular biotechnology · 2025Review
- Involvement of Oxidative Stress and Antioxidants in Modification of Cardiac Dysfunction Due to Ischemia-Reperfusion Injury.Antioxidants (Basel, Switzerland) · 2025Review
- Identification of regulator gene and pathway in myocardial ischemia-reperfusion injury: a bioinformatics and biological validation study.Hereditas · 2025Article
- Article
- Specific NOX4 Inhibition Preserves Mitochondrial Function and Dampens Kidney Dysfunction Following Ischemia-Reperfusion-Induced Kidney Injury.Antioxidants (Basel, Switzerland) · 2024Article
- Intramyocardial Injection of Hypoxia-Conditioned Extracellular Vesicles Modulates Response to Oxidative Stress in the Chronically Ischemic Myocardium.Bioengineering (Basel, Switzerland) · 2024Article
- A network pharmacology approach to decipher the mechanism of total flavonoids from Dracocephalum Moldavica L. in the treatment of cardiovascular diseases.BMC complementary medicine and therapies · 2024Article
- Knockdown of ANGPTL2 promotes left ventricular systolic dysfunction by upregulation of NOX4 in mice.Frontiers in physiology · 2024Article
- Potential Role of Natural Antioxidants in Countering Reperfusion Injury in Acute Myocardial Infarction and Ischemic Stroke.Antioxidants (Basel, Switzerland) · 2023Review
- New NADPH Oxidase 2 Inhibitors Display Potent Activity against Oxidative Stress by Targeting p22Antioxidants (Basel, Switzerland) · 2023Article
- Mitochondrial Fission as a Therapeutic Target for Metabolic Diseases: Insights into Antioxidant Strategies.Antioxidants (Basel, Switzerland) · 2023Review
- Review
- Natural Bioactive Compounds Targeting NADPH Oxidase Pathway in Cardiovascular Diseases.Molecules (Basel, Switzerland) · 2023Review
- Research progress of AMP-activated protein kinase and cardiac aging.Open life sciences · 2023Review
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 2 countries.
Funding
Abstract
Oxidative stress is critically involved in the pathophysiology of myocardial ischemic-reperfusion (I/R) injury. NADPH oxidase (Nox) 2 and 4, major sources of reactive oxygen species (ROS) in cardiomyocytes, are upregulated in response to I/R. Suppression of Nox-derived ROS prevents mitochondrial dysfunction and endoplasmic reticulum (ER) stress, leading to attenuation of myocardial I/R injury. However, minimal levels of ROS by either Nox2 or Nox4 are required for energy metabolism during I/R in the heart, preserving hypoxia-inducible factor-1α (HIF-1α) and peroxisome proliferator-activated receptor-α (PPARα) levels. Furthermore, extreme suppression of Nox activity induces reductive stress, leading to paradoxical increases in ROS levels. Nox4 has distinct roles in organelles such as mitochondria, ER, and ER-mitochondria contact sites (MAMs). Mitochondrial Nox4 exerts a detrimental effect, causing ROS-induced mitochondrial dysfunction during I/R, whereas Nox4 in the ER and MAMs is potentially protective against I/R injury through regulation of autophagy and MAM function, respectively. Although Nox isoforms are potential therapeutic targets for I/R injury, to maximize the effect of intervention, it is likely important to optimize the ROS level and selectively inhibit Nox4 in mitochondria. Here, we discuss the 'Yin and Yang' functions of Nox isoforms during myocardial I/R.
Indexed as
Identifiers
What Socratic 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 Socratic graph.