ArticleFrontiers in medicine2025
Asymmetric dimethylarginine mediates oxidative stress and atrial remodeling in HL-1 cells.
Article in Frontiers in medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Selected Nutraceuticals in Metabolic Syndrome: Molecular Mechanisms and Clinical Implications.Biomedicines · 2026Review
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3 authors.
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Abstract
Introduction: Atrial fibrillation (AF) is a common cardiac arrhythmia, and endothelial dysfunction and oxidative stress (OS) are key mechanisms promoting atrial remodeling. Asymmetric dimethylarginine (ADMA) inhibits nitric oxide synthase (NOS) but its role in AF-related atrial remodeling remains unclear. Methods: Mouse atrial myocyte HL-1 cells were treated with ADMA, H Results: ADMA (30 μM) significantly increased ROS generation and upregulated p47phox and TGF-β1 expression in HL-1 cells, which was reversed by NAC. AF patients had higher serum ADMA and TGF-β1 levels and lower NO levels than controls ( Discussion: ADMA may induce TGF-β1 expression by enhancing NOX-ROS levels, leading to myocardial oxidative damage and atrial remodeling, which provides new insights into AF pathophysiology.
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