Why the study?
Endothelial dysfunction and oxidative stress promote atrial remodeling in AF, but the role of asymmetric dimethylarginine in AF-related atrial remodeling remains unclear.
Does ADMA mediate oxidative stress and atrial remodeling in atrial myocytes and correlate with atrial fibrillation in patients?
Cohort (n=90)
No
Does ADMA mediate oxidative stress and atrial remodeling in atrial myocytes and correlate with atrial fibrillation in patients?
ADMA promotes atrial remodeling by enhancing NOX-ROS levels and inducing TGF-β1 expression, providing a potential mechanistic link to atrial fibrillation pathophysiology.
Answers are grounded in this paper and cite their sources.
Supports ADMA-mediated remodeling in AF; hypothesis-generating for therapies, should not yet change practice.
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 2 O 2 , N-acetylcysteine (NAC), or their combinations. Cell viability, reactive oxygen species (ROS) levels, and TGF-β1 expression were detected using CCK-8, flow cytometry, fluorescence microscopy, and Western blot. A clinical cohort study included 60 AF patients and 30 controls to measure serum ADMA, TGF-β1, and NO levels. 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 ( P <0.01). 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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Yu et al. (2025) conducted a cohort in Atrial fibrillation (n=90). Atrial fibrillation vs. Controls was evaluated on Serum ADMA, TGF-β1, and NO levels (p=<0.01).
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