ArticleThe Journal of clinical investigation2018
Specialized fibroblast differentiated states underlie scar formation in the infarcted mouse heart.
Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 431 papers, 1 of them a synthesis that pooled it.
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Who cites it
431 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- Human adult and pediatric multimodal transcriptomic atlas of progression from pressure-loaded to failing right ventricle.Nature cardiovascular research · 2026Article
- MMP12 induces fibrogenic macrophage differentiation to drive granuloma-associated cardiac fibrosis.American journal of respiratory and critical care medicine · 2026Article
- Fast skeletal myosin binding protein-C expression exacerbates dysfunction in heart failure.Basic research in cardiology · 2026Article
- Macrophage Mistargeting During Direct Cardiac Reprogramming: Cardiac-Associated Responses, Polarization, and Cell Death.Biomedicines · 2026Article
- Cardiac fibrosis: mechanistic insights and translational advances.Molecular biomedicine · 2026Review
- ParTIpy: a scalable framework for archetypal analysis and Pareto task inference.Molecular systems biology · 2026Article
- Coronary endothelial cells undergo venous-enriched disrupted maturation following myocardial infarction.Basic research in cardiology · 2026Article
- Establishing Primary Cultures of Adult Mouse Cardiac Fibroblasts: A Comparative Evaluation of Three Experimental Protocols.International journal of molecular sciences · 2026Article
- Review
- Ubiquitin-Related Proteostatic Programs in Cycling Fibroblast-Lineage Remodeling After Myocardial Ischemic Injury: A Hypothesis Informed by Single-Cell and Spatial Transcriptomics.International journal of molecular sciences · 2026Review
- Slick K+ channels contribute to cardiac remodeling, fibrosis, and dysfunction in postinfarction hearts.JCI insight · 2026Article
- Involvement of Fibulin-5 in endothelial to mesenchymal transition leading to cardiac fibrosis during metabolic syndrome.Journal of translational medicine · 2026Article
- Spatial and Single-Cell Mapping Reveals Valvular Interstitial Cell and Macrophage Sex Differences in Calcific Aortic Valve Disease.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Preclinical evaluation of cysteine protease-inhibitor aloxistatin (E64d) for heart failure therapy.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Molecular imaging of immune and fibrosis targets to guide therapy for repair after myocardial infarction.Nature reviews. Cardiology · 2026Review
- Salvage Third-Patch Repair for Left Ventricular Free Wall Rupture After Double-Patch Septal Reconstruction.Annals of thoracic surgery short reports · 2026Article
- The Role of the Pentose Phosphate Pathway in Cardiovascular Diseases.Cardiovascular drugs and therapy · 2026Review
- ECMSim: A high-performance interactive web application for real-time spatiotemporal simulation of cardiac ECM signaling and diffusion.Matrix biology plus · 2026Article
- TAK1 drives inflammatory fibroblast acquisition and shapes myocardial infarction responses in male mice.Nature communications · 2026Article
371 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors.
Funding
Abstract
Fibroblasts are a dynamic cell type that achieve selective differentiated states to mediate acute wound healing and long-term tissue remodeling with scarring. With myocardial infarction injury, cardiomyocytes are replaced by secreted extracellular matrix proteins produced by proliferating and differentiating fibroblasts. Here, we employed 3 different mouse lineage-tracing models and stage-specific gene profiling to phenotypically analyze and classify resident cardiac fibroblast dynamics during myocardial infarction injury and stable scar formation. Fibroblasts were activated and highly proliferative, reaching a maximum rate within 2 to 4 days after infarction injury, at which point they expanded 3.5-fold and were maintained long term. By 3 to 7 days, these cells differentiated into myofibroblasts that secreted abundant extracellular matrix proteins and expressed smooth muscle α-actin to structurally support the necrotic area. By 7 to 10 days, myofibroblasts lost proliferative ability and smooth muscle α-actin expression as the collagen-containing extracellular matrix and scar fully matured. However, these same lineage-traced initial fibroblasts persisted within the scar, achieving a new molecular and stable differentiated state referred to as a matrifibrocyte, which was also observed in the scars of human hearts. These cells express common and unique extracellular matrix and tendon genes that are more specialized to support the mature scar.
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