ArticleCardiovascular toxicology2021
Increased Susceptibility of Atrial Fibrillation Induced by Hyperuricemia in Rats: Mechanisms and Implications.
Article in Cardiovascular toxicology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed, 18 citations in OpenAlex.
- Atrial Fibrillation and Great Saphenous Vein Insufficiency: Exploration of Common Pathways in Hemodynamic Derangements and Systemic Inflammation.Reviews in cardiovascular medicine · 2026Review
- Uric Acid: A New Perspective for Exploring the Pathological Process of Anthracycline-Induced Cardiotoxicity.Current issues in molecular biology · 2025Article
- Article
- X-ray Radiotherapy Impacts Cardiac Dysfunction by Modulating the Sympathetic Nervous System and Calcium Transients.International journal of molecular sciences · 2024Article
- The Role of Hyperuricemia in Cardiac Diseases: Evidence, Controversies, and Therapeutic Strategies.Biomolecules · 2024Review
- Distinct uric acid trajectories are associated with incident cardiac conduction block.Arthritis research & therapy · 2024Article
- Notopterol Ameliorates Hyperuricemia-Induced Cardiac Dysfunction in Mice.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Association between serum uric acid levels and atrial fibrillation in different fasting glucose patterns: A case-control study.Frontiers in endocrinology · 2023Article
- Potential role of tea drinking in preventing hyperuricaemia in rats: biochemical and molecular evidence.Chinese medicine · 2022Article
- Article
- The Key Role of Uric Acid in Oxidative Stress, Inflammation, Fibrosis, Apoptosis, and Immunity in the Pathogenesis of Atrial Fibrillation.Frontiers in cardiovascular medicine · 2021Review
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High levels of serum uric acid is closely associated with atrial fibrillation (AF); nonetheless, the detailed mechanisms remain unknown. Therefore, this work examined the intricate mechanisms of AF triggered by hyperuricemia and the impact of the uricosuric agent benzbromarone on atrial remodeling in hyperuricemic rats. After adjusting baseline serum uric acid levels, a total of 28 healthy male adult Sprague Dawley rats were randomly divided into 4 groups, namely, control (CTR), hyperuricemia (oxonic acid potassium salt, OXO) and benzbromarone (+ BBR), and OXO withdrawal groups. Primary rat cardiomyocytes were cultured with uric acid for 24 h to investigate the direct influence of uric acid on cardiomyocytes. Results revealed that AF vulnerability and AF duration were dramatically greater in hyperuricemic rats (OXO group), while the atrial effective refractory periods (AERPs) were significantly shorter. Meanwhile, BBR treatment and withdrawal of 2% OXO administration remarkably reduced AF inducibility and shortened AF duration. Moreover, abnormal morphology of atrial myocytes, atrial fibrosis, apoptosis, and substantial sympathetic nerve sprouting were observed in hyperuricemic rats. Apoptosis and fibrosis of atria were partly mediated by caspase-3, BAX, TGF-β1, and α-smooth muscle actin. Uric acid significantly induced primary rat cardiomyocyte apoptosis and fibrosis in vitro. Also, we found that sympathetic nerve sprouting was markedly upregulated in the atria of hyperuricemia rats, and was restored by BRB or absence of OXO administration. In summary, our study confirmed that AF induced by hyperuricemic rats occurred primarily via induction of atrial remodeling, thereby providing a novel potential treatment approach for hyperuricemia-related AF.
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