ArticleMolecular biology of the cell2017
Mechanical regulation of cardiac fibroblast profibrotic phenotypes.
Article in Molecular biology of the cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 141 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
141 citing papers in PubMed, 195 citations in OpenAlex.
- Biomechanical stress unmasks a fibroblast-dependent hypercontractile-disarray phenotype in MYBPC3 truncation HCM.APL bioengineering · 2026Article
- Restoration of structural organization in engineered cardiac microtissues is promoted by cardiomyocyte beating.Communications biology · 2026Article
- Review
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- Cardio-Vascular Extracellular Matrix: The Unmet Enigma.International journal of molecular sciences · 2026Review
- Article
- Reprogramming the wound microenvironment: identity remodeling strategies for fibroblasts, keratinocytes, and macrophages.Frontiers in immunology · 2026Review
- The Potential Connection Between Mechanical Stress and Heart Failure with Preserved Ejection Fraction: Mechanistic Insights and Therapeutic Potential.International journal of medical sciences · 2026Review
- Precision immunomodulation of viral myocarditis: a spatiotemporal intervention paradigm based on smart biomaterials.Frontiers in immunology · 2026Review
- Substrate elasticity controls fibroblast motility on non-oxidized PDMS under weak adhesion.Biophysics and physicobiology · 2026Article
- Distinct Roles of Surface Nanostructure and Polymer Degradation in Fibroblast Response to Device Design.Research square · 2025Article
- Distinct Roles of Surface Nanostructure and Polymer Degradation in Fibroblast Response to Device Design.bioRxiv : the preprint server for biology · 2025Article
- From fibro/adipogenic progenitors to adipocytes: Understanding adipogenesis in muscle degeneration for disease modulation.The Journal of physiology · 2025Review
- Hybrid hydrogel-extracellular matrix scaffolds identify biochemical and mechanical signatures of cardiac ageing.Nature materials · 2025Article
- Characterizing the Impact of Fabrication Methods on Mechanically Tunable Gelatin Hydrogels for Cardiac Fibrosis Studies.Bioengineering (Basel, Switzerland) · 2025Article
- The Role of Cardiac Fibroblast Heterogeneity in Myocardial Fibrosis and Its Novel Therapeutic Potential.International journal of molecular sciences · 2025Review
- METTL3 Modulates Radiation-Induced Cardiac Fibrosis via the Akt/mTOR Pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Article
- The mechanobiology of fibroblast activation in disease.APL bioengineering · 2025Review
- Dressed in Collagen: 2D and 3D Cardiac Fibrosis Models.International journal of molecular sciences · 2025Review
81 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Cardiac fibrosis is a serious condition currently lacking effective treatments. It occurs as a result of cardiac fibroblast (CFB) activation and differentiation into myofibroblasts, characterized by proliferation, extracellular matrix (ECM) production and stiffening, and contraction due to the expression of smooth muscle α-actin. The mechanical properties of myocardium change regionally and over time after myocardial infarction (MI). Although mechanical cues are known to activate CFBs, it is unclear which specific mechanical stimuli regulate which specific phenotypic trait; thus we investigated these relationships using three in vitro models of CFB mechanical activation and found that 1) paracrine signaling from stretched cardiomyocytes induces CFB proliferation under mechanical conditions similar to those of the infarct border region; 2) direct stretch of CFBs mimicking the mechanical environment of the infarct region induces a synthetic phenotype with elevated ECM production; and 3) progressive matrix stiffening, modeling the mechanical effects of infarct scar maturation, causes smooth muscle α-actin fiber formation, up-regulation of collagen I, and down-regulation of collagen III. These findings suggest that myocyte stretch, fibroblast stretch, and matrix stiffening following MI may separately regulate different profibrotic traits of activated CFBs.
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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.