ArticleAmerican journal of physiology. Heart and circulatory physiology2019
Atrial fibrillation and electrophysiology in transgenic mice with cardiac-restricted overexpression of FKBP12.
Article in American journal of physiology. Heart and circulatory physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 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.
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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- Optical mapping: pioneering the frontier of preclinical antiarrhythmic drug evaluation.iScience · 2026Review
- Mechanisms underlying dilated cardiomyopathy associated with FKBP12 deficiency.The Journal of general physiology · 2025Article
- Dual effect of cardiac FKBP12.6 overexpression on excitation-contraction coupling and the incidence of ventricular arrhythmia depending on its expression level.Journal of molecular and cellular cardiology · 2024Article
- Cellular and extracellular proteomic profiling of paradoxical low-flow low-gradient aortic stenosis myocardium.Frontiers in cardiovascular medicine · 2024Article
- Hypoxia Promotes Atrial Tachyarrhythmias via Opening of ATP-Sensitive Potassium Channels.Circulation. Arrhythmia and electrophysiology · 2023Article
- Guidelines for assessment of cardiac electrophysiology and arrhythmias in small animals.American journal of physiology. Heart and circulatory physiology · 2022Review
- Research Progress of Myocardial Fibrosis and Atrial Fibrillation.Frontiers in cardiovascular medicine · 2022Review
- Inward Rectifier KJournal of the American Heart Association · 2020Article
- Article
Corrections and comments
- Erratum issuedCorrigendum.2019
Authors and funding
15 authors at 5 institutions in 3 countries.
Funding
Abstract
Cardiomyocyte-restricted overexpression of FK506-binding protein 12 transgenic (αMyHC-FKBP12) mice develop spontaneous atrial fibrillation (AF). The aim of the present study is to explore the mechanisms underlying the occurrence of AF in αMyHC-FKBP12 mice. Spontaneous AF was documented by telemetry in vivo and Langendorff-perfused hearts of αMyHC-FKBP12 and littermate control mice in vitro. Atrial conduction velocity was evaluated by optical mapping. The patch-clamp technique was applied to determine the potentially altered electrophysiology in atrial myocytes. Channel protein expression levels were evaluated by Western blot analyses. Spontaneous AF was recorded in four of seven αMyHC-FKBP12 mice but in none of eight nontransgenic (NTG) controls. Atrial conduction velocity was significantly reduced in αMyHC-FKBP12 hearts compared with NTG hearts. Interestingly, the mean action potential duration at 50% but not 90% was significantly prolonged in αMyHC-FKBP12 atrial myocytes compared with their NTG counterparts. Consistent with decreased conduction velocity, average peak Na
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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.