ArticleFrontiers in molecular biosciences2025
Metformin modulates oxidative stress via activation of AMPK/NF-κB signaling in Trisomy 21 fibroblasts: an
Article in Frontiers in molecular biosciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Dose-Dependent Genome-Wide DNA Methylation Remodeling by Metformin Modulates Doxorubicin Sensitivity in Cardiac Cells.Epigenomes · 2026Article
- Metformin as a Multifaceted Therapeutic Agent for Gastrointestinal Diseases: Mechanisms, Clinical Efficacy, and Future Directions.Pharmacology research & perspectives · 2026Review
- Loss of Proteostasis and Early-Onset Neurodegeneration in Down Syndrome: From Mechanisms to Interventions.Antioxidants (Basel, Switzerland) · 2026Review
- A Novel Protective Strategy Against Metformin-Induced Renal Injury Involving Adenosine Triphosphate and Thiamine Pyrophosphate.International journal of molecular sciences · 2026Article
- From Elixirs to Geroscience: A Historical and Molecular Perspective on Anti-Aging Medicine.Molecules (Basel, Switzerland) · 2025Review
- Evaluation of Serum Antioxidant Activity in Type 2 Diabetes and Prediabetes: Links with Nutritional and Anthropometric Factors-Preliminary Studies.Current issues in molecular biology · 2025Article
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Authors and funding
5 authors.
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Abstract
Introduction: Oxidative stress and impaired antioxidant defenses are key contributors to cellular dysfunction in Trisomy 21 (T21), highlighting the need for targeted therapeutic strategies. This study explores the modulatory effects of metformin on oxidative stress and antioxidant capacity in T21. Methods: An Results: Our results demonstrate that metformin treatment significantly reduced total oxidative capacity (TOC) and levels of oxidative DNA/RNA damage products in T21 cell lines (CCL-84 and CCL-54). Additionally, metformin markedly increased total antioxidant capacity (TAC) in these fibroblasts. Furthermore, metformin influenced key signaling pathways, as evidenced by increased levels of nuclear factor kappa B (NF-κB) and enhanced activity of protein kinase AMP-activated alpha 1 (PRKAA1) and AMP-activated protein kinase (AMPK) in T21 cell lines. Conclusions: These findings highlight metformin's significant role in modulating oxidative stress and inflammation- related mechanisms in T21. Given the growing interest in managing oxidative stress during pregnancies affected by T21, this study presents potential clinical implications for therapeutic intervention.
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