ArticleNature cardiovascular research2022
Fibroblasts orchestrate cellular crosstalk in the heart through the ECM.
Article in Nature cardiovascular research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed.
- A 3D-Bioprinted, Cell-Guiding Hydrogel Patch Promotes Functional Repair of Abdominal Incisions via Anisotropic ECM Remodeling.Smart medicine · 2026Article
- Acute Kidney Injury-to-Chronic Kidney Disease Transition-Associated Macrophage Subtypes: Biological Functions and Intercellular Crosstalk.International journal of molecular sciences · 2026Review
- Selective titin cleavage disrupts cardiac mechanical homeostasis to drive heart failure and fibrosis.Nature cardiovascular research · 2026Article
- Cardiac fibroblasts in myocardial injury and heart failure.European heart journal · 2026Review
- Modular bioreactor for multi-well electrical stimulation ofLab on a chip · 2026Article
- The immune-cardiovascular metabolic circuitry in myocardial ischemia-reperfusion injury: from metabolic signal release to spatiotemporal reprogramming.Frontiers in immunology · 2026Review
- Beyond cardiac fibroblasts: research advances on understanding and targeting intercellular communication networks in cardiac fibrosis.Frontiers in cardiovascular medicine · 2026Review
- Biomimetic electrospun scaffolds for engineered heart tissue: from design parameters to drug testing platforms.Frontiers in bioengineering and biotechnology · 2026Review
- Uridine-Cytidine Kinase 2 (UCK2)/Uridine-Cytidine Kinase Like 1 (UCKL1) complex exacerbates the differentiation of myocardial fibroblasts via TRIM21/Smurf2/Smad3 pathway after myocardial infarction.Molecular biomedicine · 2025Article
- AI-based Predictive Signaling Pathway Profiling in Cardiac Fibrosis Suggests a Novel Combinatorial Treatment Strategy.bioRxiv : the preprint server for biology · 2025Article
- Mechanical Stress Triggers Premature Senescence in Cardiac Fibroblasts.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Cardiac fibrosis: from mechanisms and models to medicines.Trends in pharmacological sciences · 2025Review
- What Is Cardiometabolic HFpEF and How Can We Study it Preclinically?JACC. Basic to translational science · 2025Review
- Interpretable machine learning coupled to spatial transcriptomics unveils mechanisms of macrophage-driven fibroblast activation in ischemic cardiomyopathy.medRxiv : the preprint server for health sciences · 2025Article
- Starvation activates ECM-remodeling gene transcription and putative enhancers in fibroblasts despite inducing quiescence.Cell reports · 2025Article
- CUGBP Elav-like family member 4 promotes cardiac remodeling through Inhibition of FMO2.BMC cardiovascular disorders · 2025Article
- Effects of embryonic origin, tissue cues and pathological signals on fibroblast diversity in humans.Nature cell biology · 2025Review
- GDF10 promotes rodent cardiomyocyte maturation during the postnatal period.Journal of molecular and cellular cardiology · 2025Article
- Dynamic molecular atlas of cardiac fibrosis at single-cell resolution shows CD248 in cardiac fibroblasts orchestrates interactions with immune cells.Nature cardiovascular research · 2025Article
- Trbp inhibits cardiac fibrosis through TGF-β pathway-mediated cross-talk between cardiomyocytes and fibroblasts.Clinical science (London, England : 1979) · 2025Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Cell communication is needed for organ function and stress responses, especially in the heart. Cardiac fibroblasts, cardiomyocytes, immune cells, and endothelial cells comprise the major cell types in ventricular myocardium that together coordinate all functional processes. Critical to this cellular network is the non-cellular extracellular matrix (ECM) that provides structure and harbors growth factors and other signaling proteins that affect cell behavior. The ECM is not only produced and modified by cells within the myocardium, largely cardiac fibroblasts, it also acts as an avenue for communication among all myocardial cells. In this Review, we discuss how the development of therapeutics to combat cardiac diseases, specifically fibrosis, relies on a deeper understanding of how the cardiac ECM is intertwined with signaling processes that underlie cellular activation and behavior.
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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.