ArticleThe European respiratory journal2025
Evidence for a lipofibroblast-to-
Article in The European respiratory journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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.
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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.
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Who cites it
23 citing papers in PubMed.
- A FGFR3 decoy receptor attenuates lung fibroblast-to-myofibroblast transition and pulmonary fibrosis.American journal of respiratory cell and molecular biology · 2026Article
- The telomeric DNA damage response as a therapeutic target in idiopathic pulmonary fibrosis.EMBO molecular medicine · 2026Article
- Non-Resolving Repair in Idiopathic Pulmonary Fibrosis: From Failed Cellular Transitions to Architectural Lock-In.International journal of molecular sciences · 2026Review
- Article
- Pulmonary fibroblast subsets demonstrate differentially enriched signaling pathways during fibrosis resolution and repair.JCI insight · 2026Article
- RUNX1 is a mediator of fibrotic activation and epigenetic memory in lung fibroblasts.American journal of respiratory cell and molecular biology · 2026Article
- Fibroblasts as regulators of lung immunity, repair and fibrosis.Nature reviews. Immunology · 2026Review
- Persistence of alveolar fibroblast-derived ADAMTS4+ cells in a preclinical model of delayed pulmonary fibrosis resolution.Nature communications · 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
- Multi-omics analysis reveals distinct spatial compartmentalization of lung repair niches in pediatric ARDS.Journal of translational medicine · 2025Article
- Prenatal lipopolysaccharide exposure programs the early-life lung development by modulating mesenchymal fibroblasts in a time- and dose-dependent manner.BMC medicine · 2025Article
- Loss of lung mesenchymal identities in culture and a screening approach to identify restorative cues.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Review
- Pathogenic expansion: fibroblast proliferation fuels fibrosis.The Journal of clinical investigation · 2025Article
- Succinic Acid-Induced Macrophage Endocytosis Promotes Extracellular Vesicle-Based Integrin Beta1 Transfer Accelerating Fibroblast Activation and Sepsis-Associated Pulmonary Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Scar wars: the viral menace.American journal of physiology. Lung cellular and molecular physiology · 2025Review
- Review
- Aging affects reprogramming of pulmonary capillary endothelial cells after lung injury in male mice.Nature communications · 2025Article
- Emerging Concepts in Fibroblast Biology and Progressive Pulmonary Fibrosis.Seminars in respiratory and critical care medicine · 2025Review
- Stromal heterogeneity in the adult lung delineated by single-cell genomics.American journal of physiology. Cell physiology · 2025Review
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34 authors.
Funding
Abstract
backgroundFibrosis is often associated with aberrant repair mechanisms that ultimately lead to organ failure. In the lung, idiopathic pulmonary fibrosis (IPF) is a fatal form of interstitial lung disease for which there is currently no curative therapy. From the cell biology point of view, the cell of origin and eventual fate of activated myofibroblasts (aMYFs) have taken centre stage, as these cells are believed to drive structural remodelling and lung function impairment. While aMYFs are now widely believed to originate from alveolar fibroblasts, the heterogeneity and ultimate fate of aMYFs during fibrosis resolution remain elusive. We have shown previously that aMYF dedifferentiation and acquisition of a lipofibroblast (LIF)-like phenotype represent a route of fibrosis resolution.
methodsIn this study, we combined genetic lineage tracing and single-cell transcriptomics in mice, and data mining of human IPF datasets to decipher the heterogeneity of aMYFs and investigate differentiation trajectories during fibrosis resolution. Furthermore, organoid cultures were utilised as a functional readout for the alveolar mesenchymal niche activity during various phases of injury and repair in mice.
resultsOur data demonstrate that aMYFs consist of four subclusters displaying unique pro-alveologenic
conclusionOur work identifies a subcluster of aMYFs that is potentially relevant for future management 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.