ArticleJournal of molecular histology2024
Halofuginone ameliorates the susceptibility to atrial fibrillation by activating the PI3K/Akt signaling pathway.
Article in Journal of molecular histology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Dopamine receptor D1 is altered in atrial fibrillation-associated tissues and modulates Ang II-induced cardiomyocyte stress partly through PI3K/Akt signaling.Molecular biology reports · 2026Article
- The impact of the PI3K/AKT pathway on arrhythmia: mechanisms of action and therapeutic potential.Journal of molecular histology · 2026Review
- Ion channels and atrial fibrillation: mitophagy as a key mediator.Frontiers in physiology · 2025Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atrial fibrillation (AF) is the most common cardiac arrhythmia in clinical practice. Halofuginone (HF) exerts beneficial effects on organ fibrosis, periodontitis, and cancer. However, the effect of HF against AF remains unknown. During the induction of AF, the rats were intragastrically administered HF (5 mg/kg and 10 mg/kg) daily for 7 consecutive days. Cardiac function was evaluated through echocardiographic analysis. The presence of pathological changes and interstitial fibrosis in the left atrial tissues were investigated. Intracellular Ca
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Registered trials
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