ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2005
NADPH oxidase-derived reactive oxygen species in cardiac pathophysiology.
Review in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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
44 citing papers in PubMed, 108 citations in OpenAlex.
- Peroxisomal catalase and plasmalogen biosynthesis protect from oxidative stress in Barth syndrome cardiomyopathy.Basic research in cardiology · 2026Article
- Review
- Redox Imbalance in the Cardiohepatic Syndrome: The Emerging Role of Oxidative Stress in Cirrhosis-Associated Cardiac Dysfunction.Antioxidants (Basel, Switzerland) · 2026Review
- Role of Reactive Oxygen Species in Collagen-Induced Platelet Activation and the Protective Effects of Antioxidants.Antioxidants (Basel, Switzerland) · 2025Article
- Exercise and dietary interventions in the management of diabetic cardiomyopathy: mechanisms and implications.Cardiovascular diabetology · 2025Review
- Role of AMPK and Sirtuins in Aging Heart: Basic and Translational Aspects.Aging and disease · 2024Review
- Modelling Diabetic Cardiomyopathy: Using Human Stem Cell-Derived Cardiomyocytes to Complement Animal Models.Metabolites · 2022Review
- The Role of Oxidative Stress in the Aging Heart.Antioxidants (Basel, Switzerland) · 2022Review
- Involvement of Oxidative Stress in the Development of Subcellular Defects and Heart Disease.Biomedicines · 2022Review
- Insulin Resistance and Vitamin D Deficiency: A Link Beyond the Appearances.Frontiers in cardiovascular medicine · 2022Review
- Effects of Estrogen on Cardiac mRNA and LncRNA Expression Profiles in Hypertensive Mice.Journal of cardiovascular translational research · 2021Article
- Sirtuin 6 Protects Against Oxidative Stress and Vascular Dysfunction in Mice.Frontiers in physiology · 2021Article
- Oxidative Stress in ESRD Patients on Dialysis and the Risk of Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2020Review
- Downregulation of PPARα during Experimental Left Ventricular Hypertrophy Is Critically Dependent on Nox2 NADPH Oxidase Signalling.International journal of molecular sciences · 2020Article
- The Ubiquitin Proteasome System in Ischemic and Dilated Cardiomyopathy.International journal of molecular sciences · 2019Article
- The attenuation of myocardial hypertrophy by atorvastatin via the intracellular calcium signal and the p38 MAPK pathway.International journal of clinical and experimental pathology · 2019Article
- Role of Endothelium in Doxorubicin-Induced Cardiomyopathy.JACC. Basic to translational science · 2018Review
- Oxidative Stress and Cardiovascular Complications in Chronic Kidney Disease, the Impact of Anaemia.Pharmaceuticals (Basel, Switzerland) · 2018Review
- Protection of Luteolin-7-O-glucoside against apoptosis induced by hypoxia/reoxygenation through the MAPK pathways in H9c2 cells.Molecular medicine reports · 2018Article
- Gallic Acid Reduces Blood Pressure and Attenuates Oxidative Stress and Cardiac Hypertrophy in Spontaneously Hypertensive Rats.Scientific reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic heart failure, secondary to left ventricular hypertrophy or myocardial infarction, is a condition with increasing morbidity and mortality. Although the mechanisms underlying the development and progression of this condition remain a subject of intense interest, there is now growing evidence that redox-sensitive pathways play an important role. This article focuses on the involvement of reactive oxygen species derived from a family of superoxide-generating enzymes, termed NADPH oxidases (NOXs), in the pathophysiology of ventricular hypertrophy, the accompanying interstitial fibrosis and subsequent heart failure. In particular, the apparent ability of the different NADPH oxidase isoforms to define the response of a cell to a range of physiological and pathophysiological stimuli is reviewed. If confirmed, these data would suggest that independently targeting different members of the NOX family may hold the potential for therapeutic intervention in the treatment of cardiac disease.
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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.