ArticleJournal of immunology (Baltimore, Md. : 1950)2014
Fibrocytes are not an essential source of type I collagen during lung fibrosis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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
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
51 citing papers in PubMed, 87 citations in OpenAlex.
- Macrophage regulation of extracellular matrix remodeling in aging skeletal muscle.Ageing research reviews · 2026Review
- Circulating Fibrocytes: Cellular Mediators of Tissue Fibrosis.International journal of molecular sciences · 2026Review
- Concomitant Idiopathic Pulmonary Fibrosis and Lung Cancer: An Updated Narrative Review.Advances in respiratory medicine · 2025Review
- Degradation of oxidized phospholipids by lysosomal phospholipase A2 regulates pulmonary fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- PIEZO1 mediates periostin+ myofibroblast activation and pulmonary fibrosis in mice.The Journal of clinical investigation · 2025Article
- CD45+/ Col I+ Fibrocytes: Major source of collagen in the fibrotic lung, but not in passaged fibroblast cultures.Matrix biology : journal of the International Society for Matrix Biology · 2025Article
- Pravastatin prevents colitis-associated carcinogenesis by reducing CX3CR1Scientific reports · 2024Article
- Understanding myofibroblast origin in the fibrotic lung.Chinese medical journal pulmonary and critical care medicine · 2024Review
- Discoidin domain receptor 2 signaling through PIK3C2α in fibroblasts promotes lung fibrosis.The Journal of pathology · 2024Article
- Genome-wide screens identify SEL1L as an intracellular rheostat controlling collagen turnover.Nature communications · 2024Article
- CD36/Lyn kinase interactions within macrophages promotes pulmonary fibrosis in response to oxidized phospholipid.Respiratory research · 2023Article
- Inhibition of discoidin domain receptor 2 reveals kinase-dependent and kinase-independent functions in regulating fibroblast activity.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- MEX3B inhibits collagen production in eosinophilic nasal polyps by downregulating epithelial cell TGFBR3 mRNA stability.JCI insight · 2023Article
- Standard of care drugs do not modulate activity of senescent primary human lung fibroblasts.Scientific reports · 2023Article
- Lung Fibrosis and Fibrosis in the Lungs: Is It All about Myofibroblasts?Biomedicines · 2022Review
- Muscarinic receptor M3 activation promotes fibrocytes contraction.Frontiers in pharmacology · 2022Article
- Molecular Mechanisms and Cellular Contribution from Lung Fibrosis to Lung Cancer Development.International journal of molecular sciences · 2021Review
- Recent developments in the pathobiology of lung myofibroblasts.Expert review of respiratory medicine · 2021Review
- Fibrocytes: A Critical Review and Practical Guide.Frontiers in immunology · 2021Review
- Dissecting the Role of Mesenchymal Stem Cells in Idiopathic Pulmonary Fibrosis: Cause or Solution.Frontiers in pharmacology · 2021Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Progressive fibrosis involves accumulation of activated collagen-producing mesenchymal cells. Fibrocytes are hematopoietic-derived cells with mesenchymal features that potentially have a unique and critical function during fibrosis. Fibrocytes have been proposed as an important direct contributor of type I collagen deposition during fibrosis based largely on fate-mapping studies. To determine the functional contribution of hematopoietic cell-derived type I collagen to fibrogenesis, we use a double-transgenic system to specifically delete the type I collagen gene across a broad population of hematopoietic cells. These mice develop a robust fibrotic response similar to littermate genotype control mice injured with bleomycin indicating that fibrocytes are not a necessary source of type I collagen. Using collagen-promoter GFP mice, we find that fibrocytes express type I collagen. However, fibrocytes with confirmed deletion of the type I collagen gene have readily detectable intracellular type I collagen indicating that uptake of collagen from neighboring cells account for much of the fibrocyte collagen. Collectively, these results clarify several seemingly conflicting reports regarding the direct contribution of fibrocytes to collagen deposition.
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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.