ArticleScientific reports2023
Growth factors and mechano-regulated reciprocal crosstalk with extracellular matrix tune the keratocyte-fibroblast/myofibroblast transition.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 23 citations in OpenAlex.
- Mechanical regulation of cell memory.Nature structural & molecular biology · 2026Review
- A Microwell Platform for Characterizing the Dynamic Response of Corneal Keratocytes to Biochemical and Biophysical Cues.Micromachines · 2026Article
- Administration of Topical NorLeuInternational journal of molecular sciences · 2026Article
- Step-Ladder Bioprinting to Align Collagen Fibers for Anisotropic Tissue Fabrication.Small (Weinheim an der Bergstrasse, Germany) · 2026Article
- Bioartificial human corneas generated by tissue engineering. A historical and technical review.Histology and histopathology · 2026Review
- Corneal Myofibroblasts Suppress T-Cell Immunity in Corneal Transplantation.Investigative ophthalmology & visual science · 2025Article
- Regulation of corneal stromal cell behavior by modulating curvature using a hydraulically-controlled organ chip array.Nature communications · 2025Article
- Single-Cell Transcriptomics Shows Cellular Heterogeneity, Intercellular Communication, and Extracellular Matrix Remodeling in Corneal Fibrosis In Vivo.Investigative ophthalmology & visual science · 2025Article
- Investigating prolactin-induced protein and its role in modulating the metabolic state of the keratoconus microenvironment.Experimental eye research · 2025Review
- Co-differentiation and enrichment of corneal endothelial cells and keratocytes from human pluripotent stem cells.Scientific reports · 2025Article
- Corneal Keratocytes, Fibroblasts, and Myofibroblasts Exhibit Distinct Transcriptional Profiles In Vitro.Investigative ophthalmology & visual science · 2025Article
- Towards predicting implant-induced fibrosis: A standardized network model of macrophage-fibroblast interactions.Computational and structural biotechnology journal · 2025Article
- Matrix glycosaminoglycans and proteoglycans in human cornea organoids and similarities with fetal corneal stages.The ocular surface · 2025Article
- Proteolysis and Contractility Regulate Tissue Opening and Wound Healing by Lung Fibroblasts in 3D Microenvironments.Advanced healthcare materials · 2024Article
- Albendazole ameliorates aerobic glycolysis in myofibroblasts to reverse pulmonary fibrosis.Journal of translational medicine · 2024Article
- Assessment and Evaluation of Contemporary Approaches for Astrocyte Differentiation from hiPSCs: A Modeling Paradigm for Alzheimer's Disease.Biological procedures online · 2024Article
- Use of a pH-responsive imatinib mesylate sustained-release hydrogel for the treatment of tendon adhesion by inhibiting PDGFRβ/CLDN1 pathway.Bioactive materials · 2024Article
- Amelioration of Fibrosis via S1P Inhibition Is Regulated by Inactivation of TGF-β and SPL Pathways in the Human Cornea.International journal of molecular sciences · 2024Article
- Delivery technologies for therapeutic targeting of fibronectin in autoimmunity and fibrosis applications.Advanced drug delivery reviews · 2024Review
- Squishy matters - Corneal mechanobiology in health and disease.Progress in retinal and eye research · 2024Review
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Improper healing of the cornea after injury, infections or surgery can lead to corneal scar formation, which is associated with the transition of resident corneal keratocytes into activated fibroblasts and myofibroblasts (K-F/M). Myofibroblasts can create an extracellular matrix (ECM) niche in which fibrosis is promoted and perpetuated, resulting in progressive tissue opacification and vision loss. As a reversion back to quiescent keratocytes is essential to restore corneal transparency after injury, we characterized how growth factors with demonstrated profibrotic effects (PDGF, FGF, FBS, TGFβ1) induce the K-F/M transition, and whether their withdrawal can revert it. Indeed, the upregulated expression of αSMA and the associated changes in cytoskeletal architecture correlated with increases in cell contractility, fibronectin (Fn) and collagen matrix density and Fn fiber strain, as revealed by 2D cell culture, nanopillar cellular force mapping and a FRET-labeled Fn tension probe. Substrate mechanosensing drove a more complete K-F/M transition reversal following growth factor withdrawal on nanopillar arrays than on planar glass substrates. Using decellularized ECM scaffolds, we demonstrated that the K-F/M transition was inhibited in keratocytes reseeded onto myofibroblast-assembled, and/or collagen-1-rich ECM. This supports the presence of a myofibroblast-derived ECM niche that contains cues favoring tissue homeostasis rather than fibrosis.
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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.