ReviewFrontiers in physiology2015
SR calcium handling dysfunction, stress-response signaling pathways, and atrial fibrillation.
Review in Frontiers in physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 11 citations in OpenAlex.
- USP10 mitigates Ang II-induced atrial remodeling and atrial fibrillation susceptibility by deubiquitinating NDUFS1.JCI insight · 2026Article
- Review
- Obesity and atrial fibrillation: a narrative review from arrhythmogenic mechanisms to clinical significance.Cardiovascular diabetology · 2023Review
- Increased Density of Endogenous Adenosine AInternational journal of molecular sciences · 2023Article
- Integrated Analysis of circRNA-miRNA-mRNA-Mediated Network and Its Potential Function in Atrial Fibrillation.Frontiers in cardiovascular medicine · 2022Article
- Transcriptional regulation of stress kinase JNK2 in pro-arrhythmic CaMKIIδ expression in the aged atrium.Cardiovascular research · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Atrial fibrillation (AF) is the most common sustained arrhythmia. It is associated with a markedly increased risk of premature death due to embolic stroke and also complicates co-existing cardiovascular diseases such as heart failure. The prevalence of AF increases dramatically with age, and aging has been shown to be an independent risk of AF. Due to an aging population in the world, a growing body of AF patients are suffering a diminished quality of life and causing an associated economic burden. However, effective pharmacologic treatments and prevention strategies are lacking due to a poor understanding of the molecular and electrophysiologic mechanisms of AF in the failing and/or aged heart. Recent studies suggest that altered atrial calcium handling contributes to the onset and maintenance of AF. Here we review the role of stress-response kinases and calcium handling dysfunction in AF genesis in the aged and failing heart.
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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.