ArticleJournal of cellular and molecular medicine2021
Nitazoxanide induced myocardial injury in zebrafish embryos by activating oxidative stress response.
Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05480878 (Clinical Study Evaluating the Efficacy of Nitazoxanide and Escitalopram as Adjuvant Therapies in Patients With Rheumatoid Arthritis), which is not on this map. Cited by 5 papers.
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.
Clinical Study Evaluating the Efficacy of Nitazoxanide and Escitalopram as Adjuvant Therapies in Patients With Rheumatoid Arthritis
Who cites it
5 citing papers in PubMed, 17 citations in OpenAlex.
- Efficacy and safety of nitazoxanide and escitalopram as adjuvant therapies in patients with rheumatoid arthritis: a randomized controlled study.European journal of clinical pharmacology · 2025Trial
- Zebrafish in Cardiovascular Disease Research: from Model to Application.International journal of biological sciences · 2026Review
- Nitazoxanide: A Drug Repositioning Compound with Potential Use in Chagas Disease in a Murine Model.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Effectiveness of Nitazoxanide and Electrolyzed Oxiding Water in Treating Chagas Disease in a Canine Model.Pharmaceutics · 2023Article
- Nitazoxanide induced myocardial injury in zebrafish embryos by activating oxidative stress response.Journal of cellular and molecular medicine · 2021Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nitazoxanide (NTZ) is a broad-spectrum antiparasitic and antiviral drug (thiazole). However, although NTZ has been extensively used, there are no reports concerning its toxicology in vertebrates. This study used the zebrafish as a vertebrate model to evaluate the safety of NTZ and to analyse the related molecular mechanisms. The experimental results showed that zebrafish embryos exposed to NTZ had cardiac malformation and dysfunction. NTZ also significantly inhibited proliferation and promoted apoptosis in cardiomyocytes. Transcriptomic analysis used compared gene expression levels between zebrafish embryos in the NTZ treatment and the control groups identified 200 upregulated genes and 232 downregulated genes. Analysis by Kyoto encyclopaedia of genes and genomes (KEGG) and gene ontology (GO) showed that signal pathways on cardiomyocyte development were inhibited while the oxidative stress pathways were activated. Further experiments showed that NTZ increased the content of reactive oxygen species (ROS) in the hearts of zebrafish. Antioxidant gadofullerene nanoparticles (GFNPs) significantly alleviated the developmental toxicity to the heart, indicating that NTZ activated the oxidative stress response to cause embryonic cardiomyocyte injury in zebrafish. This study provides evidence that NTZ causes developmental abnormalities in the cardiovascular system of zebrafish.
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Registered trials
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