ArticleNature genetics2023
Dual genetic tracing reveals a unique fibroblast subpopulation modulating cardiac fibrosis.
Article in Nature genetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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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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
47 citing papers in PubMed, 55 citations in OpenAlex.
- From cell atlases to mechanisms: bridging scRNA-seq discovery with in vivo genetics.The EMBO journal · 2026Article
- Cardiac fibroblast diversity in HFpEF: states, niches, interorgan drivers and targets.Nature reviews. Cardiology · 2026Review
- IL-1-Activated Inflammatory Cardiac Fibroblasts Exacerbate Acute Coxsackievirus B3 Myocarditis.JACC. Basic to translational science · 2026Article
- Dual recombinase-mediated genetic labeling and selective ablation of fibroblasts.Science China. Life sciences · 2026Article
- Lineage tracing from cellular heritage to disease destiny.Nature genetics · 2026Review
- Intercellular chemerin-cmklr1 couples epicardial mechanosensing to fibroblasts in pressure overload.Nature communications · 2026Article
- Neuregulin-1β Mitigates Doxorubicin-Induced Cardiotoxicity viaInternational journal of molecular sciences · 2026Article
- Article
- Screening and Validation of LTBP1 as a Key Target of Oxymatrine in Inhibiting Cardiac Fibroblast Differentiation Under High Glucose Conditions: In Vitro and Bioinformatic Studies.International journal of molecular sciences · 2026Article
- Grape Seed Oil Attenuates Myocardial Fibrosis by Inhibiting the PI3K/AKT Signaling Pathway.Foods (Basel, Switzerland) · 2026Article
- Decoding organ fibrosis: mechanistic insights and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Temporal inhibition of ADAM17 in fibroblasts reduces stiffness and promotes vascularization following myocardial infarction.Cardiovascular research · 2026Article
- Invasion of Epicardial-Derived Cells to the Trabeculae Mediated by NFPs-Fgf Signaling Regulates Ventricular Compaction.Circulation. Heart failure · 2026Article
- Luteolin and its derivatives: modulation of epithelial-mesenchymal transition in fibrosis and cancer.Frontiers in pharmacology · 2026Review
- Cardiomyocyte-derived BDNF restricts cardiac fibrosis by decreasing the activity of the TGF-β/Smad2/3 pathway and increasing Smad7 expression.Frontiers in cell and developmental biology · 2026Article
- Mesenchymal stem cell-derived extracellular vesicles: emerging cell-free therapeutics for kidney diseases.Frontiers in immunology · 2026Review
- Cardiac fibroblast heterogeneity in cardiac fibrosis implication for cell-type-specific treatment.Frontiers in physiology · 2026Review
- Article
- Exploring the impact of endocrine-disrupting chemicals on erectile dysfunction through network toxicology and machine learning.BMC pharmacology & toxicology · 2025Article
- Chronic Mitral Valve Fibrosis in Rheumatic Heart Disease: From Immune Trigger to Inflammatory and Mechanical Progression.Journal of the American Heart Association · 2025Review
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Authors and funding
21 authors at 10 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
After severe heart injury, fibroblasts are activated and proliferate excessively to form scarring, leading to decreased cardiac function and eventually heart failure. It is unknown, however, whether cardiac fibroblasts are heterogeneous with respect to their degree of activation, proliferation and function during cardiac fibrosis. Here, using dual recombinase-mediated genetic lineage tracing, we find that endocardium-derived fibroblasts preferentially proliferate and expand in response to pressure overload. Fibroblast-specific proliferation tracing revealed highly regional expansion of activated fibroblasts after injury, whose pattern mirrors that of endocardium-derived fibroblast distribution in the heart. Specific ablation of endocardium-derived fibroblasts alleviates cardiac fibrosis and reduces the decline of heart function after pressure overload injury. Mechanistically, Wnt signaling promotes activation and expansion of endocardium-derived fibroblasts during cardiac remodeling. Our study identifies endocardium-derived fibroblasts as a key fibroblast subpopulation accounting for severe cardiac fibrosis after pressure overload injury and as a potential therapeutic target against cardiac fibrosis.
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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.