ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2014
Nitrated fatty acids reverse pulmonary fibrosis by dedifferentiating myofibroblasts and promoting collagen uptake by alveolar macrophages.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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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.
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Who cites it
53 citing papers in PubMed, 77 citations in OpenAlex.
- Fibroblasts: a diverse population of cells balancing homeostasis, wound healing, regeneration, inflammation, fibrosis, and cancer across organs.JCI insight · 2026Review
- MRC2-mediated collagen internalization is reduced in fibrotic lung fibroblasts and increased upon phenotypic dedifferentiation.JCI insight · 2026Article
- Lung scRNA-seq reveals chronic inflammation and emphysemous phenotype in mice with osteogenesis imperfecta.Frontiers in genetics · 2026Article
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- Crosstalk between macrophages and immunometabolism and their potential roles in tissue repair and regeneration.Heliyon · 2024Review
- Aging of alveolar type 2 cells induced byBiomolecules & biomedicine · 2024Article
- Regulation of myofibroblast dedifferentiation in pulmonary fibrosis.Respiratory research · 2024Review
- Effects of Anti-Fibrotic Drugs on Transcriptome of Peripheral Blood Mononuclear Cells in Idiopathic Pulmonary Fibrosis.International journal of molecular sciences · 2024Article
- Pulmonary Fibrosis and Diabetes Mellitus: Two coins with the same face.Archives of internal medicine research · 2024Article
- Glycolysis and beyond in glucose metabolism: exploring pulmonary fibrosis at the metabolic crossroads.Frontiers in endocrinology · 2024Review
- Monocytes and macrophages: emerging mechanisms and novel therapeutic targets in pulmonary fibrosis.American journal of physiology. Cell physiology · 2023Review
- Simvastatin Improves Benign Prostatic Hyperplasia: Role of Peroxisome-Proliferator-Activated Receptor-γ and Classic WNT/β-Catenin Pathway.International journal of molecular sciences · 2023Article
- Cellular and Molecular Mechanisms in Idiopathic Pulmonary Fibrosis.Advances in respiratory medicine · 2023Review
- Increased expression and accumulation of GDF15 in IPF extracellular matrix contribute to fibrosis.JCI insight · 2022Article
- Fatty acid metabolism-related genes in bronchoalveolar lavage fluid unveil prognostic and immune infiltration in idiopathic pulmonary fibrosis.Frontiers in endocrinology · 2022Article
- Metabolic requirements of pulmonary fibrosis: role of fibroblast metabolism.The FEBS journal · 2021Review
- Effects of fatty acid nitroalkanes on signal transduction pathways and airway macrophage activation.Innate immunity · 2021Article
- Macrophage-derived cytokines in pneumonia: Linking cellular immunology and genetics.Cytokine & growth factor reviews · 2021Review
- Macrophage metabolic reprogramming during chronic lung disease.Mucosal immunology · 2021Review
- Ongoing Exposure to Peritoneal Dialysis Fluid Alters Resident Peritoneal Macrophage Phenotype and Activation Propensity.Frontiers in immunology · 2021Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a progressive, fatal disease, thought to be largely transforming growth factor β (TGFβ) driven, for which there is no effective therapy. We assessed the potential benefits in IPF of nitrated fatty acids (NFAs), which are unique endogenous agonists of peroxisome proliferator-activated receptor γ (PPARγ), a nuclear hormone receptor that exhibits wound-healing and antifibrotic properties potentially useful for IPF therapy. We found that pulmonary PPARγ is down-regulated in patients with IPF. In vitro, knockdown or knockout of PPARγ expression in isolated human and mouse lung fibroblasts induced a profibrotic phenotype, whereas treating human fibroblasts with NFAs up-regulated PPARγ and blocked TGFβ signaling and actions. NFAs also converted TGFβ to inactive monomers in cell-free solution, suggesting an additional mechanism through which they may inhibit TGFβ. In vivo, treating mice bearing experimental pulmonary fibrosis with NFAs reduced disease severity. Also, NFAs up-regulated the collagen-targeting factor milk fat globule-EGF factor 8 (MFG-E8), stimulated collagen uptake and degradation by alveolar macrophages, and promoted myofibroblast dedifferentiation. Moreover, treating mice with established pulmonary fibrosis using NFAs reversed their existing myofibroblast differentiation and collagen deposition. These findings raise the prospect of treating IPF with NFAs to halt and perhaps even reverse the progress of IPF.
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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.