ArticleJCI insight2018
αvβ3 Integrin drives fibroblast contraction and strain stiffening of soft provisional matrix during progressive fibrosis.
Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 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
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Who cites it
82 citing papers in PubMed, 123 citations in OpenAlex.
- Article
- Review
- Toxoplasma gondii infection reduces CD59 expression through downregulation of JAK2/STAT3 signaling axis to enhance decidual NK cell cytotoxicity via the RAS/MAPK pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Integrin-mediated mechanotransduction in the tumor microenvironment: macrophage-centered signaling mechanisms and immune remodeling.Journal of translational medicine · 2026Review
- Aligned Fibronectin Microenvironment Temporally Facilitates Profibrotic Fibroblast Activation via Integrin α5β1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- An agent-based model suggests how senescent cell behavior and matrix mechanics drive pulmonary fibrosis in aged mice.bioRxiv : the preprint server for biology · 2026Article
- Mapping cellular and ECM heterogeneity in pulmonary fibrosis - insights from recent spatiomics studies.Cell biomaterials · 2026Article
- Mechanobiology and Resolution of Lung Fibrosis.Annual review of physiology · 2026Review
- Inhalation-Based Nanoparticle Drug Delivery Targeting the Diseased Lower Airways in Idiopathic Pulmonary Fibrosis.Pharmaceutics · 2026Review
- Pulmonary-Targeted Nanoparticles Interrupt the Malignant Mechanical and Biochemical Signaling Crosstalk for Idiopathic Pulmonary Fibrosis Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Identification of Ephrin type-B receptor 4 as a critical mediator of tissue fibrosis.JCI insight · 2025Article
- Loss of MFAP5 and Its Effect on Skin Homeostasis and Wound Healing.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Tolerability and effect of inhibiting microfibrillar-associated protein 4 in small intestinal anastomotic healing.Scientific reports · 2025Article
- Endometrial Stromal Cells from Endometriosis Patients Reflect Lesion-Type-Specific Heterogeneity.Cells · 2025Article
- Article
- Fibroblast mechanoperception instructs pulmonary developmental and pattern specification gene expression programs.PLoS genetics · 2025Article
- Revisiting the biophysical aspects of extracellular-matrix-mimicking hydrogels: what cells seeBiomaterials science · 2025Review
- Lung tissue viscoelasticity is preserved with bleomycin-induced fibrosis in mice.bioRxiv : the preprint server for biology · 2025Article
- Extracellular Matrix Signaling Cues: Biological Functions, Diseases, and Therapeutic Targets.MedComm · 2025Review
- Mechanically Tunable Poly(Ethylene Glycol) Diacrylate Hydrogels Reveal Stiffness-Related Impairments in Capillary Sprouting in Experimental Lung Fibrosis.Microcirculation (New York, N.Y. : 1994) · 2025Article
22 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
9 authors at 4 institutions in 1 country.
Funding
Abstract
Fibrosis is characterized by persistent deposition of extracellular matrix (ECM) by fibroblasts. Fibroblast mechanosensing of a stiffened ECM is hypothesized to drive the fibrotic program; however, the spatial distribution of ECM mechanics and their derangements in progressive fibrosis are poorly characterized. Importantly, fibrosis presents with significant histopathological heterogeneity at the microscale. Here, we report that fibroblastic foci (FF), the regions of active fibrogenesis in idiopathic pulmonary fibrosis (IPF), are surprisingly of similar modulus as normal lung parenchyma and are nonlinearly elastic. In vitro, provisional ECMs with mechanical properties similar to those of FF activate both normal and IPF patient-derived fibroblasts, whereas type I collagen ECMs with similar mechanical properties do not. This is mediated, in part, by αvβ3 integrin engagement and is augmented by loss of expression of Thy-1, which regulates αvβ3 integrin avidity for ECM. Thy-1 loss potentiates cell contractility-driven strain stiffening of provisional ECM in vitro and causes elevated αvβ3 integrin activation, increased fibrosis, and greater mortality following fibrotic lung injury in vivo. These data suggest a central role for αvβ3 integrin and provisional ECM in overriding mechanical cues that normally impose quiescent phenotypes, driving progressive fibrosis through physical stiffening of the fibrotic niche.
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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.