ArticleThe Journal of clinical investigation2014
Resident fibroblast lineages mediate pressure overload-induced cardiac fibrosis.
Article in The Journal of clinical investigation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 404 papers.
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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
404 citing papers in PubMed.
- Regulated HSPG Signaling Directs Epicardial Behavior to Support Cardiac Formation.Circulation research · 2026Article
- From cell atlases to mechanisms: bridging scRNA-seq discovery with in vivo genetics.The EMBO journal · 2026Article
- ZEB2 SUMOylation in Cardiac Fibroblast Drives Post-Infarction Cardiac Remodeling through CtBP1-Associated repression of Nr4a1.iScience · 2026Article
- Cardiac fibroblast diversity in HFpEF: states, niches, interorgan drivers and targets.Nature reviews. Cardiology · 2026Review
- Natural Products Targeting Myocardial Fibrosis: Pharmacological Basis, Molecular Mechanisms and Translational Barriers.International journal of molecular sciences · 2026Review
- Cardiac immunity and heart repair: Mechanism, challenge, and future direction.Chinese medical journal · 2026Review
- CD34Histology and histopathology · 2026Review
- IL-1-Activated Inflammatory Cardiac Fibroblasts Exacerbate Acute Coxsackievirus B3 Myocarditis.JACC. Basic to translational science · 2026Article
- Cerebrovascular vulnerability and fibrosis in human brain aneurysms.Nature neuroscience · 2026Article
- Lineage tracing from cellular heritage to disease destiny.Nature genetics · 2026Review
- Segmental specification of the human female fetal reproductive tract revealed by spatiotemporal dynamics.Nature cell biology · 2026Article
- Vein graft failure: Pathophysiology, detection, prevention and emerging therapeutic strategies.Pharmacological reviews · 2026Review
- Intercellular chemerin-cmklr1 couples epicardial mechanosensing to fibroblasts in pressure overload.Nature communications · 2026Article
- Ameliorating post-infarction myocardial fibrosis and cardiac function via ROS-responsive hydrogel-mediated IL-11 antibody delivery.Bioactive materials · 2026Article
- Genetic drivers of congenital cardiac fibrosis.Communications biology · 2026Review
- Leptin Receptor Fibroblasts Are Preferential Contributors to Cardiac Fibrosis.Circulation research · 2026Article
- Microvascular endothelial scavenger receptor class B type I protects against heart failure with preserved ejection fraction by inhibiting T-cell cardiotropism.EMBO molecular medicine · 2026Article
- PW1Stem cell research & therapy · 2026Article
- Protective Role of Hesperidin Against Deltamethrin-Induced Cardiovascular Structural Damage: Involvement of Caspase-3-Driven Apoptosis and Fibrosis Suppression in Rats.Journal of cardiovascular development and disease · 2026Article
- An innovative in vitro model for studying the biology of cardiac fibroblasts originating from the epicardium.Disease models & mechanisms · 2026Article
344 more citing papers are in PubMed but not listed here.
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16 authors.
Funding
Abstract
Activation and accumulation of cardiac fibroblasts, which result in excessive extracellular matrix deposition and consequent mechanical stiffness, myocyte uncoupling, and ischemia, are key contributors to heart failure progression. Recently, endothelial-to-mesenchymal transition (EndoMT) and the recruitment of circulating hematopoietic progenitors to the heart have been reported to generate substantial numbers of cardiac fibroblasts in response to pressure overload-induced injury; therefore, these processes are widely considered to be promising therapeutic targets. Here, using multiple independent murine Cre lines and a collagen1a1-GFP fusion reporter, which specifically labels fibroblasts, we found that following pressure overload, fibroblasts were not derived from hematopoietic cells, EndoMT, or epicardial epithelial-to-mesenchymal transition. Instead, pressure overload promoted comparable proliferation and activation of two resident fibroblast lineages, including a previously described epicardial population and a population of endothelial origin. Together, these data present a paradigm for the origins of cardiac fibroblasts during development and in fibrosis. Furthermore, these data indicate that therapeutic strategies for reducing pathogenic cardiac fibroblasts should shift from targeting presumptive EndoMT or infiltrating hematopoietically derived fibroblasts, toward common pathways upregulated in two endogenous fibroblast populations.
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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.