Trial reportDrugs in R&D2013
N-Acetylcysteine effects on transforming growth factor-β and tumor necrosis factor-α serum levels as pro-fibrotic and inflammatory biomarkers in patients following ST-segment elevation myocardial infarction.
Trial report in Drugs in R&D, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- N-Acetylcysteine for Cardiac Protection During Coronary Artery Reperfusion: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.Frontiers in cardiovascular medicine · 2021Pooled it
- Complement C3c as a biomarker in heart failure.Mediators of inflammation · 2013Trial
- Inactivation of Notch1-TGF-β-Smads Signaling Pathway by Atorvastatin Improves Cardiac Function and Hemodynamic Performance in Acute Myocardial Infarction Rats.Journal of vascular research · 2025Article
- The Role of Pro-Inflammatory Cytokines in the Pathogenesis of Cardiovascular Disease.International journal of molecular sciences · 2024Review
- Review
- Signaling pathways and targeted therapy for myocardial infarction.Signal transduction and targeted therapy · 2022Review
- The Value of Serum YKL-40 and TNF-Cardiology research and practice · 2022Article
- Reduction of Activin Receptor-Like Kinase 4 Expression Ameliorates Myocardial Ischemia/Reperfusion Injury through Inhibiting TGFAnalytical cellular pathology (Amsterdam) · 2022Article
- Communication Between Cardiomyocytes and Fibroblasts During Cardiac Ischemia/Reperfusion and Remodeling: Roles of TGF-β, CTGF, the Renin Angiotensin Axis, and Non-coding RNA Molecules.Frontiers in physiology · 2021Review
- Therapeutic Efficacy of Antioxidants in Ameliorating Obesity Phenotype and Associated Comorbidities.Frontiers in pharmacology · 2020Review
- Antinociceptive and anti-inflammatory effects of N-acetylcysteine and verapamil in Wistar rats.The Korean journal of pain · 2019Article
- Article
- A Multi-Trait Approach Identified Genetic Variants Including a Rare Mutation in RGS3 with Impact on Abnormalities of Cardiac Structure/Function.Scientific reports · 2019Article
- Transforming growth factor β and its role in heart disease.Experimental and therapeutic medicine · 2017Article
- N-acetylcysteine attenuates the development of cardiac fibrosis and remodeling in a mouse model of heart failure.Physiological reports · 2016Article
- A new Agkistrodon halys venom-purified protein C activator prevents myocardial fibrosis in diabetic rats.Croatian medical journal · 2015Article
- N-acetylcysteine Plus Deferoxamine Improves Cardiac Function in Wistar Rats After Non-reperfused Acute Myocardial Infarction.Journal of cardiovascular translational research · 2015Article
- Good and bad sides of TGFβ-signaling in myocardial infarction.Frontiers in physiology · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
aimsIschemia following acute myocardial infarction (AMI) increases the level of pro-fibrotic and inflammatory cytokines, including transforming growth factor (TGF)-β and tumor necrosis factor (TNF)-α. N-acetylcysteine (NAC) has therapeutic benefits in the management of patients with AMI. To the best of our knowledge, this is the first study that has evaluated the effect of NAC on TNF-α and TGF-β levels in patients with AMI.
methodsFollowing confirmation of AMI, 88 patients were randomly administered NAC 600 mg (Fluimucil(®), Zambon, Ticino, Switzerland) or placebo orally twice daily for 3 days. For quantification of TGF-β and TNF-α serum levels after 24 and 72 h of NAC or placebo administration, peripheral venous blood (10 mL) samples were collected at these time points.
resultsComparisons between levels of TGF-β and TNF-α after 24 and 72 h within the NAC or placebo groups revealed that there was not any significant difference except for TGF-β levels in the placebo group, which increased significantly over time (p = 0.042). Significant relationships existed between patients' ejection fraction (p = 0.005) and TGF-β levels.
conclusionsReceiving NAC could prevent TGF-β levels from increasing after 72 h as compared with not receiving NAC. As TGF-β had strong correlations with the ejection fraction, its antagonism seems to be important in the prevention of remodeling.
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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.