ReviewAntioxidants (Basel, Switzerland)2025
Endothelial Dysfunction: Redox Imbalance, NLRP3 Inflammasome, and Inflammatory Responses in Cardiovascular Diseases.
Review in Antioxidants (Basel, Switzerland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 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
59 citing papers in PubMed, 1 synthesis or guideline pooled it.
- A Systematic Review of Endothelial Dysfunction in Chronic Venous Disease-Inflammation, Oxidative Stress, and Shear Stress.International journal of molecular sciences · 2025Pooled it
- Boron as a Context-Dependent System-Level Modulator: Mechanisms and Implications in Chronic Diseases.Biological trace element research · 2026Review
- Pulsatility as a Potential Regulator of Cardiovascular Biology: Molecular, Cellular, and Hemodynamic Remodeling During Continuous-Flow Left Ventricular Assist Device Support and Following Heart Transplantation.International journal of molecular sciences · 2026Review
- Review
- Microvesicle-Derived Redox Signatures as Mediators of Endothelial Dysfunction in Diabetes.International journal of molecular sciences · 2026Article
- Crosstalk of thioredoxin system and programmed cell death: from pathophysiology to novel therapy.Redox biology · 2026Review
- Role of NLRP3 Inflammasome Inhibitors in Endothelial Dysfunction and Vascular Repair.Antioxidants (Basel, Switzerland) · 2026Review
- Inflammaging Beyond Biomarkers: Molecular Mechanisms and Therapeutic Opportunities.Current issues in molecular biology · 2026Review
- Carotid Intima-Media Thickness and Atherogenic Indices in Idiopathic Pulmonary Fibrosis: Evidence of Subclinical Atherosclerosis.Life (Basel, Switzerland) · 2026Article
- The Bidens pilosa extract Jacein alleviates hypertension by restoring mitochondrial dynamic balance through modulating the FAM210A/OPA1 signaling pathway.Molecular and cellular biochemistry · 2026Article
- Superoxide Dismutase-Centered Modulation by Curcumin in Cardiovascular Diseases: Mechanistic Insights and Translational Implications.Journal of cellular and molecular medicine · 2026Review
- Cardiovascular Toxicity of BTKi in Chronic B-Cell Malignancies.Reviews in cardiovascular medicine · 2026Review
- Insights in ischemia/reperfusion injury and cardioprotection: neglected and emerging pathways and therapeutic targets for a personalized therapy.Basic research in cardiology · 2026Review
- Hormonal Shifts and Structural Strain: A Literature Review of Menopause and Perimenopause in Relation to Overuse Injuries and Stress Fractures.Annals of rehabilitation medicine · 2026Article
- EndMT in vascular cognitive impairment and dementia: mechanisms, evidence gaps, and therapeutic opportunities.Molecular medicine (Cambridge, Mass.) · 2026Review
- Protective mechanism of sevoflurane preconditioning on myocardial ischemia-reperfusion injury by regulating RMRP/miR-206 axis.BMC pharmacology & toxicology · 2026Article
- Urinary Albumin-to-Creatinine Ratio as an Independent Predictor of 90-Day Outcomes in Patients Hospitalized for Acute Decompensated Heart Failure.Journal of clinical medicine · 2026Article
- Multi-omics data mining combined with experimental validation reveals ferroptosis- and autophagy-associated hub genes as diagnostic candidates and immune modulators in atherosclerosis.Animal models and experimental medicine · 2026Article
- Associations of Lipid and Adiposity Indices with Vascular Aging Stages in a Multicenter Chinese Population.Current medical science · 2026Article
- Review
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endothelial dysfunction (ED) is characterized by an imbalance between vasodilatory and vasoconstrictive factors, leading to impaired vascular tone, thrombosis, and inflammation. These processes are critical in the development of cardiovascular diseases (CVDs) such as atherosclerosis, hypertension and ischemia/reperfusion injury (IRI). Reduced nitric oxide (NO) production and increased oxidative stress are key contributors to ED. Aging further exacerbates ED through mitochondrial dysfunction and increased oxidative/nitrosative stress, heightening CVD risk. Antioxidant systems like superoxide-dismutase (SOD), glutathione-peroxidase (GPx), and thioredoxin/thioredoxin-reductase (Trx/TXNRD) pathways protect against oxidative stress. However, their reduced activity promotes ED, atherosclerosis, and vulnerability to IRI. Metabolic syndrome, comprising insulin resistance, obesity, and hypertension, is often accompanied by ED. Specifically, hyperglycemia worsens endothelial damage by promoting oxidative stress and inflammation. Obesity leads to chronic inflammation and changes in perivascular adipose tissue, while hypertension is associated with an increase in oxidative stress. The NLRP3 inflammasome plays a significant role in ED, being triggered by factors such as reactive oxygen and nitrogen species, ischemia, and high glucose, which contribute to inflammation, endothelial injury, and exacerbation of IRI. Treatments, such as N-acetyl-L-cysteine, SGLT2 or NLRP3 inhibitors, show promise in improving endothelial function. Yet the complexity of ED suggests that multi-targeted therapies addressing oxidative stress, inflammation, and metabolic disturbances are essential for managing CVDs associated with metabolic syndrome.
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What Socratic 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 Socratic graph.