ArticleCurrent pathobiology reports2017
Heterogeneity of Fibroblasts and Myofibroblasts in Pulmonary Fibrosis.
Article in Current pathobiology reports, 2017. 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, 90 citations in OpenAlex.
- Comparative Transcriptomics of Feather Follicles Reveals Potential Candidate Genes for Duck Feather Type Differentiation.Animals : an open access journal from MDPI · 2026Article
- Pulmonary fibroblast subsets demonstrate differentially enriched signaling pathways during fibrosis resolution and repair.JCI insight · 2026Article
- Macropinocytosis inhibition attenuates profibrotic responses in lung fibroblasts and pulmonary fibrosis models.The Journal of clinical investigation · 2026Article
- Transcriptional and spatial profiling of fibroblasts from human lungs highlights CTHRC1+ cells as fibrogenic signaling hubs in fibrosis.bioRxiv : the preprint server for biology · 2026Article
- Transcriptomic responses of lung mesenchymal cells during pneumonia.JCI insight · 2025Article
- Local, Quantitative Morphometry of Fibroproliferative Lung Injury Using Laminin.American journal of respiratory cell and molecular biology · 2024Article
- Highlighting fibroblast plasticity in lung fibrosis: the WI-38 cell line as a model for investigating the myofibroblast and lipofibroblast switch.Theranostics · 2024Article
- Article
- Exercise training attenuates angiotensin II-induced cardiac fibrosis by reducing POU2F1 expression.Journal of sport and health science · 2023Article
- Regulating the cell shift of endothelial cell-like myofibroblasts in pulmonary fibrosis.The European respiratory journal · 2023Article
- Early events marking lung fibroblast transition to profibrotic state in idiopathic pulmonary fibrosis.Respiratory research · 2023Article
- Retinoids stored locally in the lung are required to attenuate the severity of acute lung injury in male mice.Nature communications · 2023Article
- The Regenerative Power of Stem Cells: Treating Bleomycin-Induced Lung Fibrosis.Stem cells and cloning : advances and applications · 2023Review
- Invadosome Formation by Lung Fibroblasts in Idiopathic Pulmonary Fibrosis.International journal of molecular sciences · 2022Article
- Pulmonary Fibrosis as a Result of Acute Lung Inflammation: Molecular Mechanisms, Relevant In Vivo Models, Prognostic and Therapeutic Approaches.International journal of molecular sciences · 2022Review
- TRPM7 restrains plasmin activity and promotes transforming growth factor-β1 signaling in primary human lung fibroblasts.Archives of toxicology · 2022Article
- Functional Repercussions of Hypoxia-Inducible Factor-2α in Idiopathic Pulmonary Fibrosis.Cells · 2022Review
- Kasugamycin Is a Novel Chitinase 1 Inhibitor with Strong Antifibrotic Effects on Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2022Article
- Anti-Fibrotic Effect of SDF-1β Overexpression in Bleomycin-Injured Rat Lung.Pharmaceutics · 2022Article
- Wound healing, fibroblast heterogeneity, and fibrosis.Cell stem cell · 2022Review
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
Abstract
purpose of reviewIdiopathic Pulmonary Fibrosis (IPF) is the most common form of interstitial lung diseases of unknown eathiopathogenesis, mean survival of 3-5 years and limited therapeutics. Characterized by a loss of alveolar type II epithelial cells and aberrant activation of stromal cells, considerable effort was undertaken to characterize the origin and activation mechanisms of fibroblasts and myofibroblasts in IPF lungs. In this review, the origin and contribution of fibroblast and myofibroblasts in lung fibrosis will be summarized. RECENT
findingsLineage tracing experiments suggested that interstitial lung fibroblasts and lipofibroblasts, pericytes and mesothelial cells differentiate into myofibroblasts. However, epithelial and bone marrow derived cells may give rise to collagen expressing fibroblasts but do not differentiate into myofibroblasts. SUMMARY: There is great heterogeneity in fibroblasts and myofibroblasts in fibrotic lungs. Further, there is evidence for the expansion of pericyte derived myofibroblasts and loss of lipofibroblasts and lipofibroblast derived myofibroblasts in IPF.
Indexed as
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.