ArticleNature communications2025
SNAP25-dependent membrane trafficking of the Kv1.5 channel regulates the onset of atrial fibrillation.
Article in Nature communications, 2025. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Emerging Regulatory Mechanisms in Sinoatrial Node Automaticity.Journal of cellular and molecular medicine · 2026Review
- Selective inhibition of LY294002 across cloned human cardiac ion channels: implications for atrium-selective therapy in atrial fibrillation.Frontiers in pharmacology · 2026Article
- PGC-1α Regulates Exercise Intensity-Dependent Atrial Remodeling and Fibrillation in Rats.Aging and disease · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors.
Funding
Abstract
Synaptosomal-associated protein 25 kDa (SNAP25) is essential for vesicular trafficking and protein docking at presynaptic membranes in the nervous system, yet its role in the heart remains poorly understood. Here, we show an unrecognized function of SNAP25, which is selectively expressed in the atria, in regulating atrial electrical remodeling and the onset of atrial fibrillation (AF). SNAP25 protein is downregulated in the atria of AF patients. Cardiomyocyte-specific knockout of SNAP25 in male mice significantly shortens the atrial effective refractory period and action potential duration (APD), increasing susceptibility to AF, which is attributed to elevated Kv1.5 current and membrane expression. Blocking Kv1.5 channels effectively restores atrial APD and reduces AF incidence. Mechanistically, SNAP25 deficiency reduces the internalization of Kv1.5 from the cell surface membrane to early endosomes. In human iPSC-derived atrial cardiomyocytes, SNAP25 deficiency similarly elevates arrhythmic activity and accelerates repolarization. In conclusion, this study reveals that SNAP25 regulates AF susceptibility by controlling the trafficking of the atrial-specific Kv1.5 channel, highlighting SNAP25 as a promising therapeutic target for atrial arrhythmias.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.