ReviewFree radical biology & medicine2011
Cysteine/cystine redox signaling in cardiovascular disease.
Review in Free radical biology & medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 142 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
142 citing papers in PubMed, 1 synthesis or guideline pooled it, 434 citations in OpenAlex.
- Effects of perioperative oxygen concentration on oxidative stress in adult surgical patients: a systematic review.British journal of anaesthesia · 2021Pooled it
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- Association Between Plasma and Urinary Reduced Thiols in Essential Hypertension: Evidence from a Paired Observational Study.Journal of clinical medicine · 2026Article
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- Redirecting Intermediary Metabolism to Counteract Cyanide Poisoning.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Review
- Sulfide regulation and catabolism in health and disease.Signal transduction and targeted therapy · 2025Review
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- On-Off-On Fluorometric Detection of Hg(II) and L-Cysteine Using Red Emissive Nitrogen-Doped Carbon Dots for Environmental and Clinical Sample Analysis.Journal of fluorescence · 2025Article
- Products of Selenite/Thiols Interaction Have Reducing Properties, Cleave Plasmid DNA and Decrease Rat Blood Pressure and Tension of Rat Mesenteric Artery.Biological trace element research · 2025Article
- Polymorphic and Expressional Analysis of GenesInternational journal of hypertension · 2025Article
- Synthesis and Characterization of Novel Co(III)/Ru(II) Heterobimetallic Complexes as Hypoxia-Activated Iron-Sequestering Anticancer Prodrugs.Molecules (Basel, Switzerland) · 2024Article
- α4 Nicotinic Acetylcholine Receptors in Lipopolysaccharide-Related Lung Inflammation.International journal of molecular sciences · 2024Article
- A facile, catalyst- and additive-free, and scalable approach to the photochemical preparation of disulfides from organosulfenyl chlorides.RSC advances · 2024Article
- Dicobalt(ii) helices kill colon cancer cellsChemical science · 2024Article
- Plasma metabolites are altered before and after diagnosis of preeclampsia or fetal growth restriction.Scientific reports · 2024Article
- Predictive effect of thiol/disulfide homeostasis dynamics on early pregnancy viability: A case-control study.Turkish journal of obstetrics and gynecology · 2024Article
- Association between healthy dietary patterns and markers of oxidative stress in the Sister Study.European journal of nutrition · 2024Article
82 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Extracellular thiol/disulfide redox environments are highly regulated in healthy individuals. The major thiol/disulfide redox couple in human plasma is cysteine (Cys) and its disulfide form, cystine (CySS). Oxidation of this redox couple, measured as a more positive steady-state redox potential (E(h)), is associated with risk factors for cardiovascular disease (CVD), including aging, smoking, obesity, and alcohol abuse. Rodent and vascular cell studies show that the extracellular redox state of Cys/CySS (E(h)CySS) can play a vital role in controlling CVD through proinflammatory signaling. This inflammatory signaling is regulated by cell-surface protein redox state and involves mitochondrial oxidation, nuclear factor-κB activation, and elevated expression of genes for monocyte recruitment to endothelial cells. Gene array and proteomics studies reveal the global nature of redox effects, and different cell types, e.g., endothelial cells, monocytes, fibroblasts, and epithelial cells, show cell-specific redox responses with different phenotypic traits, e.g., proliferation and apoptosis, which can contribute to CVD. The critical nature of the proinflammatory redox signaling and cell biology associated with E(h)CySS supports the use of plasma levels of Cys, CySS, and E(h)CySS as key indicators of vascular health. Plasma redox-state-based pharmacologic interventions to control or improve E(h)CySS may be effective in preventing CVD onset or progression.
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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.