ReviewBritish journal of pharmacology2017
Crosstalk of mitochondria with NADPH oxidase via reactive oxygen and nitrogen species signalling and its role for vascular function.
Review in British journal of pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 155 papers, 1 of them a synthesis that pooled it.
What it found
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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
155 citing papers in PubMed, 1 synthesis or guideline pooled it, 264 citations in OpenAlex.
- Exploring the role of oxidative stress in retinal vein occlusion: an updated and comprehensive review on the pathophysiology and treatment perspectives.International ophthalmology · 2025Pooled it
- Blocking mitochondrial cyclophilin D ameliorates TSH-impaired defensive barrier of artery.Redox biology · 2018Trial
- Peroxisomal catalase and plasmalogen biosynthesis protect from oxidative stress in Barth syndrome cardiomyopathy.Basic research in cardiology · 2026Article
- Experimental workflows for the accurate identification of mitochondrial redox events.Redox biology · 2026Review
- Toll-like receptor 2 impacts small intestinal villus capillarization through epithelial dual oxidase 2.Redox biology · 2026Article
- Therapeutic evaluation of artocarpin-enriched extract from Artocarpus heterophyllus heartwood in multiple sclerosis rat model.Inflammopharmacology · 2026Article
- Protein glycoxidation in neuropsychiatric disorders-from basic research to clinical practice.Redox biology · 2026Review
- Treml4 Drives Microglial Activation via the Lyn/Syk/ERK Pathway in Sepsis-Associated Encephalopathy.Neurochemical research · 2026Article
- EndMT in vascular cognitive impairment and dementia: mechanisms, evidence gaps, and therapeutic opportunities.Molecular medicine (Cambridge, Mass.) · 2026Review
- α-MSH Induces Intracellular ROS Generation in Melanoma Cells through NADPH Oxidase-1/4 Activation.Biomolecules & therapeutics · 2026Article
- The core mechanism of hypertension-linked renal fibrosis: "RAAS-ROS-inflammation-fibrosis" axis.iScience · 2026Review
- <p>Pathological mechanism of ferroptosis in a rat model of α‑naphthyl isothiocyanate‑induced chronic cholestasis</p>.Molecular medicine reports · 2026Article
- Molecular and Cellular Mechanisms of Myocardial Ischemia and Reperfusion Injury: A Narrative Review.Cells · 2026Review
- Monoamine oxidases are mediators of oxidative stress in human varicose Veins: interactions with obesity, inflammation, and angiotensin II.Molecular and cellular biochemistry · 2026Article
- Prenatal Alcohol Exposure and Mitochondrial Function in the Brain.Advances in experimental medicine and biology · 2026Review
- Oxidative Stress, Mitochondrial Homeostasis, and Sirtuins in Atrial Fibrillation.International journal of molecular sciences · 2025Review
- Identification of potential biomarkers associated with mitochondrial oxidative stress in idiopathic pulmonary arterial hypertension via bioinformatic and experimental analysis.Scientific reports · 2025Article
- Endothelial MerTK impairment accelerates the development of atherosclerosis.Redox biology · 2025Article
- Enzymatic Spirulina Extract Enhances the Vasodilation in Aorta and Mesenteric Arteries of Aged Rats.Marine drugs · 2025Article
- Modern antidiabetic therapy by sodium-glucose cotransporter 2 inhibitors, glucagon-like peptide 1 receptor agonists, and dipeptidyl peptidase 4 inhibitors against cardiovascular diseases.Pharmacological reviews · 2025Review
95 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
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiovascular diseases are associated with and/or caused by oxidative stress. This concept has been proven by using the approach of genetic deletion of reactive species producing (pro-oxidant) enzymes as well as by the overexpression of reactive species detoxifying (antioxidant) enzymes leading to a marked reduction of reactive oxygen and nitrogen species (RONS) and in parallel to an amelioration of the severity of diseases. Likewise, the development and progression of cardiovascular diseases is aggravated by overexpression of RONS producing enzymes as well as deletion of antioxidant RONS detoxifying enzymes. Thus, the consequences of the interaction (redox crosstalk) of superoxide/hydrogen peroxide produced by mitochondria with other ROS producing enzymes such as NADPH oxidases (Nox) are of outstanding importance and will be discussed including the consequences for endothelial nitric oxide synthase (eNOS) uncoupling as well as the redox regulation of the vascular function/tone in general (soluble guanylyl cyclase, endothelin-1, prostanoid synthesis). Pathways and potential mechanisms leading to this crosstalk will be analysed in detail and highlighted by selected examples from the current literature including hypoxia, angiotensin II-induced hypertension, nitrate tolerance, aging and others. The general concept of redox-based activation of RONS sources via "kindling radicals" and enzyme-specific "redox switches" will be discussed providing evidence that mitochondria represent key players and amplifiers of the burden of oxidative stress. LINKED ARTICLES: This article is part of a themed section on Redox Biology and Oxidative Stress in Health and Disease. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.12/issuetoc.
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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.