ArticleMolecular therapy : the journal of the American Society of Gene Therapy2016
Chop Deficiency Protects Mice Against Bleomycin-induced Pulmonary Fibrosis by Attenuating M2 Macrophage Production.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04849104 (Cohort Study of Airway Microecology and the Pathogenesis and Evolution of Chronic Obstructive Pulmonary Disease), which is not on this map. Cited by 136 papers.
What it found
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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.
Cohort Study of Airway Microecology and the Pathogenesis and Evolution of Chronic Obstructive Pulmonary Disease
Who cites it
136 citing papers in PubMed, 257 citations in OpenAlex.
- Plasma apolipoprotein E protein attenuates pulmonary fibrosis through LRP1 and PLAU dual receptor-mediated TGF-β/Smad inhibition.Journal of advanced research · 2026Article
- Endoplasmic reticulum stress and the unfolded protein response in lung diseases: molecular pathways and therapeutic interventions.The Journal of pathology · 2026Review
- Programmed Cell Death in Chronic Rhinosinusitis.Clinical and translational allergy · 2026Review
- Treatment of pulmonary fibrosis: From disease mechanisms to future novel therapies (Review).International journal of molecular medicine · 2026Review
- Kynurenine-AhR-SLC39A10-ZnCell communication and signaling : CCS · 2026Article
- The Transcription Factor DDIT3 Regulates Macrophage Function by Inhibiting KLF10 to Attenuate ALI/ARDS Inflammation.Inflammation · 2026Article
- Decoding Dysregulation of DNA Methylation in Epigenetics of Idiopathic Pulmonary Fibrosis.Canadian respiratory journal · 2026Review
- Mitochondrial DNA released from pyroptotic synovial macrophages via DDIT3-mediated mitophagy aggravates osteoarthritis progression.Journal of orthopaedic translation · 2026Article
- T Cell Exhaustion and Dendritic Cell-Mediated Tertiary Lymphoid Structures (TLSs) Modulation Affect Response to Neoadjuvant Chemoradiotherapy in Microsatellite Stable Rectal Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The Role of C/EBP-Homologous Protein in Idiopathic Inflammatory Myopathies.Journal of cellular and molecular medicine · 2025Article
- The critical role of LRG1 in pathological fibrosis.Journal of molecular medicine (Berlin, Germany) · 2025Review
- Exploring the Cellular and Molecular Landscape of Idiopathic Pulmonary Fibrosis: Integrative Multi-Omics and Single-Cell Analysis.Biomedicines · 2025Article
- Chop Deficiency Exacerbates Cyclophosphamide-Induced Overactive Bladder via Impaired Macrophage Apoptosis.Current medical science · 2025Article
- Inhibition of AXL ameliorates pulmonary fibrosisThe European respiratory journal · 2025Article
- The PERK/ATF4 pathway is required for metabolic reprogramming and progressive lung fibrosis.JCI insight · 2025Article
- Piperlongumine Inhibits Lung Cancer Growth by Inducing Endoplasmic Reticulum Stress Leading to Suppression of M2 Macrophage Polarization.Biological procedures online · 2025Article
- Kynurenine acts as a signaling molecule to attenuate pulmonary fibrosis by enhancing the AHR-PTEN axis.Journal of advanced research · 2025Article
- Mechanisms and Therapeutic Potential of Myofibroblast Transformation in Pulmonary Fibrosis.Journal of respiratory biology and translational medicine · 2025Article
- ADAM17/PTGS2 Facilitates Pulmonary Fibrosis by Regulating Ferroptosis.Journal of cellular and molecular medicine · 2025Article
- The role of oxidative stress-related genes in idiopathic pulmonary fibrosis.Scientific reports · 2025Article
76 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
20 authors at 5 institutions in 2 countries.
Funding
Abstract
C/EBP homologous protein (Chop) has been shown to have altered expression in patients with idiopathic pulmonary fibrosis (IPF), but its exact role in IPF pathoaetiology has not been fully addressed. Studies conducted in patients with IPF and Chop(-/-) mice have dissected the role of Chop and endoplasmic reticulum (ER) stress in pulmonary fibrosis pathogenesis. The effect of Chop deficiency on macrophage polarization and related signalling pathways were investigated to identify the underlying mechanisms. Patients with IPF and mice with bleomycin (BLM)-induced pulmonary fibrosis were affected by the altered Chop expression and ER stress. In particular, Chop deficiency protected mice against BLM-induced lung injury and fibrosis. Loss of Chop significantly attenuated transforming growth factor β (TGF-β) production and reduced M2 macrophage infiltration in the lung following BLM induction. Mechanistic studies showed that Chop deficiency repressed the M2 program in macrophages, which then attenuated TGF-β secretion. Specifically, loss of Chop promoted the expression of suppressors of cytokine signaling 1 and suppressors of cytokine signaling 3, and through which Chop deficiency repressed signal transducer and activator of transcription 6/peroxisome proliferator-activated receptor gamma signaling, the essential pathway for the M2 program in macrophages. Together, our data support the idea that Chop and ER stress are implicated in IPF pathoaetiology, involving at least the induction and differentiation of M2 macrophages.
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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.