ReviewInflammation research : official journal of the European Histamine Research Society ... [et al.]2017
Myofibroblast repair mechanisms post-inflammatory response: a fibrotic perspective.
Review in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 71 citations in OpenAlex.
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- Healed Perforated Corneal Ulcers in Human.Life (Basel, Switzerland) · 2025Article
- Is it really descemetocele? Morphology of extremely thin membrane that remained after severe corneal melting: a case report.Medical molecular morphology · 2025Article
- BRD4: an effective target for organ fibrosis.Biomarker research · 2024Review
- Inhibitor of PD-1/PD-L1: a new approach may be beneficial for the treatment of idiopathic pulmonary fibrosis.Journal of translational medicine · 2024Review
- Nanocarrier-Mediated Delivery of MicroRNAs for Fibrotic Diseases.Molecular diagnosis & therapy · 2024Review
- Upregulation of Piezo2 in the mesangial, renin, and perivascular mesenchymal cells of the kidney of Dahl salt-sensitive hypertensive rats and its reversal by esaxerenone.Hypertension research : official journal of the Japanese Society of Hypertension · 2023Article
- Article
- Blockade of the pentraxin 3/CD44 interaction attenuates lung injury-induced fibrosis.Clinical and translational medicine · 2022Article
- Myopia Development in Tree Shrew Is Associated with Chronic Inflammatory Reactions.Current issues in molecular biology · 2022Article
- Inhaled siRNA nanoparticles targetingScience advances · 2022Article
- Controllable graphene oxide-based biocompatible hybrid interface as an anti-fibrotic coating for metallic implants.Materials today. Bio · 2022Article
- Human outgrowth knee fibroblasts from patients undergoing total knee arthroplasty exhibit a unique gene expression profile and undergo myofibroblastogenesis upon TGFβ1 stimulation.Journal of cellular biochemistry · 2022Article
- Effect of crudeVeterinary world · 2022Article
- Review
- Changes of local microenvironment and systemic immunity after acupuncture stimulation during inflammation: A literature review of animal studies.Frontiers in neurology · 2022Review
- Hopes and Hurdles of Employing Mesenchymal Stromal Cells in the Treatment of Cardiac Fibrosis.International journal of molecular sciences · 2021Review
- Computational reconstruction of the signalling networks surrounding implanted biomaterials from single-cell transcriptomics.Nature biomedical engineering · 2021Article
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 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionFibrosis is a complex chronic disease characterized by a persistent repair response. Its pathogenesis is poorly understood but it is typically the result of chronic inflammation and maintained with the required activity of transforming growth factor-β (TGFβ) and extracellular matrix (ECM) tension, both of which drive fibroblasts to transition into a myofibroblast phenotype.
findingsAs the effector cells of repair, myofibroblasts migrate to the site of injury to deposit excessive amounts of matrix proteins and stimulate high levels of contraction. Myofibroblast activity is a decisive factor in whether a tissue is properly repaired by controlled wound healing or rendered fibrotic by deregulated repair. Extensive studies have documented the various contributing factors to an abrogated repair response. Though these fibrotic factors are known, very little is understood about the opposing antifibrotic molecules that assist in a successful repair, such as prostaglandin E2 (PGE
conclusionsThe idea is to understand the ways in which the cell, after an injury and inflammatory response, normally controls its repair mechanisms through its homeostatic regulators so as to mimic them therapeutically to control abnormal pathways.
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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.