Article in The Journal of physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
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.
2 · The registry
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.
Project 3 (Mercola)P01HL141084 · NHLBI · STANFORD UNIVERSITY · PI MARK MERCOLA · 2019 to 2026
$21.1M
Development of the Predictive NeuroCardiovascular SimulatorOT2OD026580 · OD · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CLANCY, COLLEEN E, GRANDI, ELEONORA · 2018 to 2021
$5.7M
The Role of Inflammasome in the Pathogenesis of Atrial FibrillationR01HL136389 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI Na Li · 2017 to 2026
$5.6M
Sex-specific arrhythmogenic mechanisms of atrial fibrillationR01HL131517 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Eleonora Grandi · 2016 to 2026
$5.0M
Functional Microdomains in the Heart's Pacemaker: A New Dimension of Cardiac RemodelingR01HL141214 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI Alexey V Glukhov · 2018 to 2026
$3.8M
Systems Pharmacology Model of Cardiac HypertrophyR01HL162925 · NHLBI · UNIVERSITY OF VIRGINIA · PI SAUCERMAN, JEFFREY J., WOLF, MATTHEW J · 2022 to 2025
$3.1M
Multiomics and Functional Characterization Establish Druggable Targets for PVC-Driven Idiopathic VFR01HL170521 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI Lee Lochbaum Eckhardt, Eleonora Grandi · 2023 to 2026
$3.1M
Resolution of inflammation and atrial fibrillationR01HL165704 · NHLBI · UNIVERSITY OF MINNESOTA · PI SAMUEL C DUDLEY · 2023 to 2026
$2.9M
Cardiac fibroblast inflammasome and atrial myopathyR01HL163277 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI LI, NA · 2022 to 2025
$2.8M
Role of Nucleoside-Diphosphate Kinase Signaling in Atrial FibrillationR01HL160992 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI Xander H.T. Wehrens · 2023 to 2026
$2.1M
Phosphodiesterase 1 (PDE1) Regulation of Myocardial Calcium and FunctionR01HL171586 · NHLBI · LOYOLA UNIVERSITY CHICAGO · PI Grace Kim Muller · 2024 to 2026
$1.9M
Phenotype-specific models, mechanisms, and treatment of HFpEFR01HL171057 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Stefano Morotti · 2024 to 2026
$1.8M
American Heart Association-American Stroke Association 20POST35120462 - HAIBO NIAmerican Heart Association-American Stroke Association 24CDA1258695American Heart Association Career Development 24CDA1258695American Heart Association Postdoctoral Fellowship 20POST35120462American Heart Association Postdoctoral Fellowship 25POST1356871Deutsche Forschungsgemeinschaft Research Training Group 2989European Union large-scale network 965 286National Institute of Aging R03AG086695National Institutes of Health Stimulating Peripheral Activity to Relieve Conditions 1OT2OD026580-01NHLBI NIH HHS P01 HL141084NHLBI NIH HHS P01HL141084NHLBI NIH HHS R00 HL138160NHLBI NIH HHS R00HL138160NHLBI NIH HHS R01 HL131517NHLBI NIH HHS R01HL131517NHLBI NIH HHS R01 HL136389NHLBI NIH HHS R01HL136389NHLBI NIH HHS R01 HL141214NHLBI NIH HHS R01HL141214NHLBI NIH HHS R01 HL160992NHLBI NIH HHS R01HL160992NHLBI NIH HHS R01 HL162925NHLBI NIH HHS R01HL162925NHLBI NIH HHS R01 HL163277NHLBI NIH HHS R01HL163277NHLBI NIH HHS R01 HL164838NHLBI NIH HHS R01HL164838NHLBI NIH HHS R01 HL165704NHLBI NIH HHS R01HL165704NHLBI NIH HHS R01 HL170521NHLBI NIH HHS R01HL170521NHLBI NIH HHS R01 HL171057NHLBI NIH HHS R01HL171057NHLBI NIH HHS R01 HL171586NHLBI NIH HHS R01HL171586NHLBI NIH HHS R01HL172417NHLBI NIH HHS R01 HL176651NHLBI NIH HHS R01HL176651NHLBI NIH HHS R01 HL176700NIA NIH HHS R03 AG086695NIH HHS OT2 OD026580
6 · The paper itself
Abstract
Atrial fibrillation (AF) is the most common arrhythmia, characterized by irregular atrial electrical activity resulting in asynchronous atrial contraction. AF is accompanied by extensive structural remodelling of atria, including extracellular matrix expansion (fibrosis), which affects both AF maintenance and treatment outcomes. However, no fibrosis-specific therapies are currently available for AF. To identify the prominent pathways in atrial fibroblasts (Fb) that modulate atrial fibrosis and arrhythmogenesis, we developed the first atrial Fb signalling network model. This expands on the well-established ventricular model by integrating atrial-relevant elements involved in fibrogenesis and/or differentially expressed in chronic AF (vs. normal sinus rhythm) patients and connections based on experimental evidence in an Fb-related context. Our findings indicate that under high profibrotic signals, e.g. angiotensin-II (AngII) and transforming growth factor β, inhibition of Ca
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.
Computational modelling of cardiac fibroblast signalling reveals a key role for Ca · full record | OpenQuestion