ReviewFrontiers in pharmacology2026
The role of ubiquitination in the pathogenesis of atrial fibrillation: mechanisms and therapeutic implications.
Review in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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8 authors.
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Abstract
Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia, defined by rapid and irregular atrial activation. Despite advances in AF treatment, AF remains a leading cause of cardiovascular morbidity and mortality worldwide. Emerging evidence demonstrates that ubiquitination, a dynamic post-translational modification, acts as a central regulator of AF pathogenesis by modulating inflammatory signaling, calcium dysregulation, ferroptosis, oxidative stress, and autophagy. This review systematically explores the multifaceted roles of ubiquitin-related enzymes (E3 ligases and deubiquitinating enzymes, DUBs) in AF pathogenesis, with an emphasis on their interactions with core molecular pathways. Furthermore, we discuss potential therapeutic strategies targeting the ubiquitin-proteasome system, and provide a framework for future translational research in AF.
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