ArticleJournal of molecular and cellular cardiology2016
Cell-specific effects of Nox2 on the acute and chronic response to myocardial infarction.
Article in Journal of molecular and cellular cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.
- Lomitapide: navigating cardiovascular challenges with innovative therapies.Molecular biology reports · 2024Pooled it
- Evaluation of neutrophil oxidative burst capacity in relation to major adverse cardiac events and infection in patients with cardiovascular disease.Clinical research in cardiology : official journal of the German Cardiac Society · 2026Article
- Cardiomyocyte Rac1 signaling in hypertrophy, arrhythmia, and cardiac stress adaptation.Journal of molecular and cellular cardiology plus · 2025Review
- Multifaceted roles of neutrophils in cardiac disease.Journal of leukocyte biology · 2025Review
- The functions of immune system-derived miRNAs in cardiovascular diseases.Non-coding RNA research · 2025Review
- The Dual Role of Oxidative Stress in Atherosclerosis and Coronary Artery Disease: Pathological Mechanisms and Diagnostic Potential.Antioxidants (Basel, Switzerland) · 2025Review
- Delineating the NOX-Mediated Promising Therapeutic Strategies for the Management of Various Cardiovascular Disorders: A Comprehensive Review.Current vascular pharmacology · 2025Review
- Very low-density lipoprotein receptor mediates triglyceride-rich lipoprotein-induced oxidative stress and insulin resistance.American journal of physiology. Heart and circulatory physiology · 2024Article
- Modulation of NOX2 causes obesity-mediated atrial fibrillation.The Journal of clinical investigation · 2024Article
- NADPH Oxidase 3: Beyond the Inner Ear.Antioxidants (Basel, Switzerland) · 2024Review
- Redox Regulation of PTEN by Reactive Oxygen Species: Its Role in Physiological Processes.Antioxidants (Basel, Switzerland) · 2024Review
- Raspberry polyphenols target molecular pathways of heart failure.The Journal of nutritional biochemistry · 2024Article
- Interplay between energy metabolism and NADPH oxidase-mediated pathophysiology in cardiovascular diseases.Frontiers in pharmacology · 2024Review
- Non-Coding RNAs in Cell-to-Cell Communication: Exploiting Physiological Mechanisms as Therapeutic Targets in Cardiovascular Pathologies.International journal of molecular sciences · 2023Review
- Interleukin 32 participates in cardiomyocyte-induced oxidative stress, inflammation and apoptosis during hypoxia/reoxygenation via the NOD2/NOX2/MAPK signaling pathway.Experimental and therapeutic medicine · 2022Article
- Role of oxidative stress in calcific aortic valve disease and its therapeutic implications.Cardiovascular research · 2022Review
- Review
- Polymeric nanoparticles in the diagnosis and treatment of myocardial infarction: Challenges and future prospects.Materials today. Bio · 2022Review
- A Retinoic Acid ReceptorThe Journal of pharmacology and experimental therapeutics · 2021Article
- Oxidative Stress Links Aging-Associated Cardiovascular Diseases and Prostatic Diseases.Oxidative medicine and cellular longevity · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
backgroundIncreased reactive oxygen species (ROS) production is involved in the process of adverse cardiac remodeling and development of heart failure after myocardial infarction (MI). NADPH oxidase-2 (Nox2) is a major ROS source within the heart and its activity increases after MI. Furthermore, genetic deletion of Nox2 is protective against post-MI cardiac remodeling. Nox2 levels may increase both in cardiomyocytes and endothelial cells and recent studies indicate cell-specific effects of Nox2, but it is not known which of these cell types is important in post-MI remodeling. METHODS AND
resultsWe have generated transgenic mouse models in which Nox2 expression is targeted either to cardiomyocytes (cardio-Nox2TG) or endothelial cells (endo-Nox2TG). We here studied the response of cardio-Nox2TG mice, endo-Nox2TG mice and matched wild-type littermates (WT) to MI induced by permanent left coronary artery ligation up to 4weeks. Initial infarct size assessed by magnetic resonance imaging (MRI) and cardiac dysfunction were similar among groups. Cardiomyocyte hypertrophy and interstitial fibrosis were augmented in cardio-Nox2TG compared to WT after MI and post-MI survival tended to be worse whereas endo-Nox2TG mice showed no significant difference compared to WT.
conclusionsThese results indicate that cardiomyocyte rather than endothelial cell Nox2 may have the more important role in post-MI remodeling.
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.