ArticleThe Journal of clinical investigation2022
TGF-β1-induced endothelial-mesenchymal transition: a potential contributor to fibrotic remodeling in atrial fibrillation?
Article in The Journal of clinical investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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.
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
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- The transcriptional landscape of atrial fibrillation: A systematic review and meta-analysis.PloS one · 2025Pooled it
- Cross-Propagative Graph Learning Reveals Spatial Tissue Domains in Multi-Modal Spatial Transcriptomics.Small methods · 2026Article
- Cellular and molecular cross-talk in atrial fibrillation: The role of non-cardiomyocytes in creating an arrhythmogenic substrate.The Journal of physiology · 2026Review
- Artificial Intelligence in the Diagnosis and Management of Atrial Fibrillation.Diagnostics (Basel, Switzerland) · 2025Review
- A Conserved FABP5Liver international : official journal of the International Association for the Study of the Liver · 2025Article
- Ubiquitin-specific protease 38 modulates atrial fibrillation susceptibility in chronic kidney disease via STRAP stabilization and activation of TGF-β/SMAD signaling.Molecular medicine (Cambridge, Mass.) · 2025Article
- Ubiquitin-specific protease 38 modulates atrial fibrillation susceptibility in chronic kidney disease via STRAP stabilization and activation of TGF-β/SMAD signaling.Molecular medicine (Cambridge, Mass.) · 2025Article
- Angiogenesis in Atrial Fibrillation: A Literature Review.Biomedicines · 2025Review
- LncRNA Dleu2 Serve as a Novel Biomarker for Ablation Recurrence and Promote Atrial Remodelling by Targeting Nr4a1 in Atrial Fibrillation.Journal of cellular and molecular medicine · 2025Article
- Possible Risk Factors Contributing to Atrial Fibrillation Occurrence in Heart Failure With Mildly Reduced Ejection Fraction.Journal of clinical medicine research · 2024Article
- The role of cellular senescence in profibrillatory atrial remodelling associated with cardiac pathology.Cardiovascular research · 2024Article
- Pathophysiology and clinical relevance of atrial myopathy.Basic research in cardiology · 2024Review
- COMP Improves Ang-II-Induced Atrial Fibrillation via TGF-β Signaling Pathway.Cardiovascular toxicology · 2023Article
- Diversity of cells and signals in the cardiovascular system.The Journal of physiology · 2023Article
- microRNAs as Biomarkers of Endothelial Dysfunction and Therapeutic Target in the Pathogenesis of Atrial Fibrillation.International journal of molecular sciences · 2023Review
- Biglycan Involvement in Heart Fibrosis: Modulation of Adenosine 2A Receptor Improves Damage in Immortalized Cardiac Fibroblasts.International journal of molecular sciences · 2023Article
- Effects of scutellarin on the mechanism of cardiovascular diseases: a review.Frontiers in pharmacology · 2023Review
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 4 countries.
Funding
Abstract
Atrial fibrillation (AF) is the most common cardiac arrhythmia worldwide, with an unmet therapeutic need. Fibrotic remodeling, in which collagen-producing atrial fibroblasts play a crucial role, substantially contributes to arrhythmia promotion and progression. In this issue of the JCI, Lai, Tsai, and co-authors reveal that TGF-β1 promoted endothelial-mesenchymal transition during AF and put forward the notion that, in the adult heart, atrial fibroblasts can originate from different cellular sources. These important findings extend our understanding of the origin, biology, and function of fibroblasts and offer possibilities for therapeutic targeting of fibrosis in AF.
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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.