ReviewMatrix biology : journal of the International Society for Matrix Biology2018
Matrix biomechanics and dynamics in pulmonary fibrosis.
Review in Matrix biology : journal of the International Society for Matrix Biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
53 citing papers in PubMed.
- Fibronectin's tensional state as a mechanical signature of fibrotic extracellular matrix in idiopathic pulmonary fibrosis models.Matrix biology plus · 2026Article
- Versican regulating viscoelasticity drives pleural fibrosis via mechanotransductive signaling.JCI insight · 2026Article
- The Piezo1-Ca2+-PI3k/Akt signaling axis as a context-dependent mechanotransduction node during skin wound healing.iScience · 2026Review
- SYISL promotes pulmonary epithelial-mesenchymal transition and fibrosis through DSP-Hippo/YAP pathway.Cellular and molecular life sciences : CMLS · 2026Article
- Myeloperoxidase promotes fibrosis by inhibiting cathepsin K to bias the lung toward ECM accumulation.bioRxiv : the preprint server for biology · 2026Article
- Mechanobiology and Resolution of Lung Fibrosis.Annual review of physiology · 2026Review
- Yifei Decoction Regulates the NGF/TRKA/PI3K/AKT Signaling Axis to Inhibit the Epithelial-Mesenchymal Transformation and Proliferation of Pulmonary Epithelial Cells in Bleomycin-Induced Pulmonary Fibrogenesis.Canadian respiratory journal · 2026Article
- The importance of mechanical forces in chronic respiratory diseases.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Review
- Insight into the pathogenesis of interstitial lung diseases and near-to-native lung fibrosis models.European journal of medical research · 2025Review
- Review
- Updated insights on ASK1 signaling: mechanisms, regulation, and therapeutic potential in diseases.Molecular and cellular biochemistry · 2025Review
- The mechanobiology of fibroblast activation in disease.APL bioengineering · 2025Review
- LncRNA SYISL promotes fibroblast myofibroblast transition via miR-23a-mediated TRIOBP regulation.Cellular and molecular life sciences : CMLS · 2025Article
- Acute contact with profibrotic macrophages mechanically activates fibroblasts via αvβ3 integrin-mediated engagement of Piezo1.Science advances · 2024Article
- Monomeric compounds from natural products for the treatment of pulmonary fibrosis: a review.Inflammopharmacology · 2024Review
- Biomechanical Properties and Cellular Responses in Pulmonary Fibrosis.Bioengineering (Basel, Switzerland) · 2024Review
- Imaging at the nexus: how state of the art imaging techniques can enhance our understanding of cancer and fibrosis.Journal of translational medicine · 2024Review
- Discoidin domain receptor 2 signaling through PIK3C2α in fibroblasts promotes lung fibrosis.The Journal of pathology · 2024Article
- Modeling mechanical activation of macrophages during pulmonary fibrogenesis for targeted anti-fibrosis therapy.Science advances · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
The composition and mechanical properties of the extracellular matrix are dramatically altered during the development and progression of pulmonary fibrosis. Recent evidence indicates that these changes in matrix composition and mechanics are not only end-results of fibrotic remodeling, but active participants in driving disease progression. These insights have stimulated interest in identifying the components and physical aspects of the matrix that contribute to cell activation and disease initiation and progression. This review summarizes current knowledge regarding the biomechanics and dynamics of the ECM in mouse models and human IPF, and discusses how matrix mechanical and compositional changes might be non-invasively assessed, therapeutically targeted, and biologically restored to resolve fibrosis.
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Identifiers
What OpenQuestion holds
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.