ReviewNature reviews. Cardiology2025
Reactive oxygen species in hypertension.
Review in Nature reviews. Cardiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 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
70 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- Plasma proteomics analysis of vitamin C supplementation in people with type 2 diabetes.Nutrition & diabetes · 2026Trial
- Gut-immune-PVAT axis is involved in ethanol-induced abdominal aortic dysfunction via IL-17RA, TLR4, and FPR1 signaling.Gut microbes · 2026Article
- Sex Differences and Oxidative Stress in Cardiovascular Disease.Physiology (Bethesda, Md.) · 2026Review
- Renin-Angiotensin Signaling and Vascular Function: Insights into Health and Disease.Acta physiologica (Oxford, England) · 2026Review
- Review
- Association Between Blood Heavy Metals and Selenium with All-Cause Mortality in Cardiovascular-Kidney-Metabolic Syndrome Populations: Exploring the Mediating Effects of Inflammatory Biomarkers.Cardiovascular toxicology · 2026Article
- Hypertensive mt. tRNARedox biology · 2026Article
- Neuroinflammation in Alzheimer's and Parkinson's diseases: pathogenic mechanisms and therapeutic strategies.Translational neurodegeneration · 2026Review
- Review
- Article
- Impact of obstructive sleep apnoea on nocturnal blood pressure: mechanisms and treatment responses - a narrative review.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Reverse cardio-oncology: neuroendocrine axis activation and cardiovascular-disease-derived factors synergistically remodel the tumor microenvironment.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- Interacting and joint impact of oxidative balance score and insulin resistance on cardiovascular and metabolic diseases risks: a cross-sectional, population-based study.BMC cardiovascular disorders · 2026Article
- Stagnant oxidative potential in declining agricultural fleets: Evidence from key particulate matter composition despite fleet renewal.Eco-Environment & Health · 2026Article
- Article
- Functionalized boron nitride nanomaterials: Exploring antioxidant and antitumor activities for advanced therapeutic applications.iScience · 2026Article
- Guidelines for evaluating endothelial function in vascular tissue.American journal of physiology. Heart and circulatory physiology · 2026Review
- The core mechanism of hypertension-linked renal fibrosis: "RAAS-ROS-inflammation-fibrosis" axis.iScience · 2026Review
- Elucidating the Role of Oxidative Stress-Associated Genes FKBP Prolyl Isomerase 5 in Osteoarthritis Development and Immunological Milieu.Biological procedures online · 2026Article
10 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
4 authors.
Funding
Abstract
Hypertension is a leading risk factor for stroke, heart disease and chronic kidney disease. Multiple interacting factors and organ systems increase blood pressure and cause target-organ damage. Among the many molecular elements involved in the development of hypertension are reactive oxygen species (ROS), which influence cellular processes in systems that contribute to blood pressure elevation (such as the cardiovascular, renal, immune and central nervous systems, or the renin-angiotensin-aldosterone system). Dysregulated ROS production (oxidative stress) is a hallmark of hypertension in humans and experimental models. Of the many ROS-generating enzymes, NADPH oxidases are the most important in the development of hypertension. At the cellular level, ROS influence signalling pathways that define cell fate and function. Oxidative stress promotes aberrant redox signalling and cell injury, causing endothelial dysfunction, vascular damage, cardiovascular remodelling, inflammation and renal injury, which are all important in both the causes and consequences of hypertension. ROS scavengers reduce blood pressure in almost all experimental models of hypertension; however, clinical trials of antioxidants have yielded mixed results. In this Review, we highlight the latest advances in the understanding of the role and the clinical implications of ROS in hypertension. We focus on cellular sources of ROS, molecular mechanisms of oxidative stress and alterations in redox signalling in organ systems, and their contributions to hypertension.
Indexed as
Identifiers
39048744What 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.