ReviewHuman genetics2020
The molecular genetic basis of atrial fibrillation.
Review in Human genetics, 2020. 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, 9 citations in OpenAlex.
- A novel PRRX1 loss-of-function variation contributing to familial atrial fibrillation and congenital patent ductus arteriosus.Genetics and molecular biology · 2022Article
- Hub microRNAs and genes in the development of atrial fibrillation identified by weighted gene co-expression network analysis.BMC medical genomics · 2021Article
- Article
- In Silico Assessment of Class I Antiarrhythmic Drug Effects onInternational journal of molecular sciences · 2021Article
- Multicohort Metabolomics Analysis Discloses 9-Decenoylcarnitine to Be Associated With Incident Atrial Fibrillation.Journal of the American Heart Association · 2021Article
- Multiomics Analysis of Genetics and Epigenetics Reveals Pathogenesis and Therapeutic Targets for Atrial Fibrillation.BioMed research international · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
As the most common cardiac arrhythmia, atrial fibrillation (AF) is a major risk factor for stroke, heart failure, and premature death with considerable associated costs. However, no available treatment options have optimal benefit-harm profiles currently, reflecting an incomplete understanding of the biological mechanisms underlying this complex arrhythmia. Recently, molecular epidemiological studies, especially genome-wide association studies, have emphasized the substantial genetic component of AF etiology. A comprehensive mapping of the genetic underpinnings for AF can expand our knowledge of AF mechanism and further facilitate the process of locating novel therapeutics for AF. Here we provide a state-of-the-art review of the molecular genetics of AF incorporating evidence from linkage analysis and candidate gene, as well as genome-wide association studies of common variations and rare copy number variations; potential epigenetic modifications (e.g., DNA methylation, histone modification, and non-coding RNAs) are also involved. We also outline the challenges in mechanism investigation and potential future directions in this article.
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.