ReviewCurrent rheumatology reports2018
Matrix Stiffness: the Conductor of Organ Fibrosis.
Review in Current rheumatology reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers, 2 of them syntheses that pooled it.
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
93 citing papers in PubMed, 2 syntheses or guidelines pooled it, 173 citations in OpenAlex.
- The rise and evolution of cancer mechanobiology: a bibliometric trajectory of three decades of research.Frontiers in pharmacology · 2026Pooled it
- Mechanisms of Peritoneal Fibrosis: Focus on Immune Cells-Peritoneal Stroma Interactions.Frontiers in immunology · 2021Pooled it
- Lipid Uptake by Alveolar Macrophages Drives Fibrotic Responses to Silica Dust.Scientific reports · 2019Trial
- Breaking the cycle of fibrosis: Ferroptosis as a therapeutic target (Review).International journal of molecular medicine · 2026Review
- Article
- Fibroblasts as regulators of lung immunity, repair and fibrosis.Nature reviews. Immunology · 2026Review
- Aortic carboxypeptidase-like protein potentiates β1 integrin signaling in mesenchymal progenitors.Life science alliance · 2026Article
- CD248 acts as a mechanosensory switch in fibroblast subsets to establish distinct pathological niches in renal fibrosis.Nature communications · 2026Article
- Mechanobiology in Stem Cell-Based Bioprinting.Cell proliferation · 2026Review
- Mechanical gating of tendon fibrogenic transcription in systemic sclerosis.Nature communications · 2026Article
- Smart hydrogel systems for skin fibrosis: rational design, mechanisms and therapeutic applications.Regenerative biomaterials · 2026Review
- Review
- Fibroblast-specific palladin drives kidney fibrosis via MRTF-SRF signaling.The Journal of pathology · 2026Article
- Emerging concepts and novel mechanisms in organ fibrosis.NPJ Regenerative medicine · 2025Article
- Lung tissue viscoelasticity is preserved with bleomycin-induced fibrosis in mice.bioRxiv : the preprint server for biology · 2025Article
- Durotaxis is a driver and potential therapeutic target in lung fibrosis and metastatic pancreatic cancer.Nature cell biology · 2025Article
- The mechanobiology of fibroblast activation in disease.APL bioengineering · 2025Review
- Renal Implications of Dysregulated Protein Homeostasis: Insights into Ubiquitin-Proteasome and Autophagy Systems.Biomolecules · 2025Review
- Epidermal stem cell derived exosomes-induced dedifferentiation of myofibroblasts inhibits scarring via the miR-203a-3p/PIK3CA axis.Journal of nanobiotechnology · 2025Article
- Peritoneal Dialysis -Associated Fibrosis: Emerging Mechanisms and Therapeutic Opportunities.Frontiers in pharmacology · 2025Review
33 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
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purpose of reviewOrgan fibrosis is a lethal component of scleroderma. The hallmark of scleroderma fibrosis is extensive extracellular matrix (ECM) deposition by activated myofibroblasts, specialized hyper-contractile cells that promote ECM remodeling and matrix stiffening. The purpose of this review is to discuss novel mechanistic insight into myofibroblast activation in scleroderma. RECENT
findingsMatrix stiffness, traditionally viewed as an end point of organ fibrosis, is now recognized as a critical regulator of tissue fibrogenesis that hijacks the normal physiologic wound-healing program to promote organ fibrosis. Here, we discuss how matrix stiffness orchestrates fibrosis by controlling three fundamental pro-fibrotic mechanisms: (a) mechanoactivation of myofibroblasts, (b) integrin-mediated latent transforming growth factor beta 1 (TGF-β1) activation, and (c) activation of non-canonical TGF-β1 signaling pathways. We also summarize novel therapeutic targets for anti-fibrotic therapy based on the mechanobiology of scleroderma. Future research on mechanobiology of scleroderma may lead to important clinical applications such as improved diagnosis and treatment of patients with scleroderma and other fibrotic-related diseases.
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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.