ArticleJournal of the American Heart Association2025
Persistent Fibrosis in Heart Failure With a Reduced Ejection Fraction Linked to Phenotypic Differences in Human Cardiac Fibroblast Populations.
Article in Journal of the American Heart Association, 2025. 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
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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.
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Who cites it
6 citing papers in PubMed.
- Mechanical stretch reduces fibroblast activation in heart failure with reduced ejection fraction.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2026Article
- Plasma proteomic signatures of cellular aging predict human disease.Nature medicine · 2026Article
- Cellular Aging Signatures in the Plasma Proteome Record Human Health and Disease.bioRxiv : the preprint server for biology · 2026Article
- Septin4 Regulates Cardiac Fibrosis After Pressure Overload.Circulation research · 2025Article
- Organ fibrosis: beyond collagen I expression. Fibroblast phenotype and basement membrane proteins.American journal of physiology. Cell physiology · 2025Review
- Fibroblast growth factor 9 activates fibroblast activation and drives the progress of shoulder stiffness.Frontiers in cell and developmental biology · 2025Article
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
backgroundMyocardial fibrosis is prevalent in cardiomyopathies that result in heart failure with reduced ejection fraction. Heart failure with reduced ejection fraction treated with a left ventricular assist device (LVAD) yields hemodynamic unloading and may provide partial cardiomyocyte recovery, but contemporary studies reveal no consistent reductions in fibrosis. This study tested the hypothesis that, despite normalization of hemodynamic overload by LVAD, fibrosis and fibroblast activation persist resulting in sustained increases in myocardial stiffness. METHODS AND
resultsTissues from subjects with heart failure with reduced ejection fraction undergoing LVAD implantation (pre-LVAD), from transplanted hearts with LVAD (post-LVAD) or without cardiac pathology (control) were collected. Quantification of myocardial stiffness and collagen content revealed significant increases in pre-LVAD versus control that remained elevated in post-LVAD. Myocardial fibroblast populations increased in pre- and post-LVAD hearts versus control. Control, pre-LVAD, and post-LVAD fibroblasts were isolated and plated on substrates with mechanical stiffnesses reflective of normal (≈2 kPa) or fibrotic (≈8 kPa) myocardium. Quantification of collagen I and α-smooth muscle actin production demonstrated that control fibroblasts were responsive to substrate stiffness, whereas pre- and post-LVAD fibroblasts were unresponsive and exhibited no significant differences on either substrate. Bulk-RNA sequence analysis revealed changes in gene expression in pre-LVAD versus control fibroblasts including mechano-sensitive pathways that appear to be uncoupled, resulting in increased expression of genes implicated in proliferation, whereas mechano-sensing genes were decreased.
conclusionsThese data support that sustained cardiac hemodynamic overload leads to a phenotypic conversion in fibroblasts in which the capacity to detect changes in mechanical input is muted, thus contributing to retention of collagen content and stiffness in both pre- and post-LVAD hearts.
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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 Socratic graph.