ArticlePloS one2019
Macrophage PPAR-γ suppresses long-term lung fibrotic sequelae following acute influenza infection.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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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Who cites it
30 citing papers in PubMed, 42 citations in OpenAlex.
- FGF8 alleviates LPS-induced acute lung injuryAnnals of medicine · 2026Article
- An aerosolized dual-action autotaxin inhibitor-PPARγ agonist for the treatment of pulmonary fibrosis.Cell reports. Medicine · 2026Article
- Type 2 immune history imprints local training in nerve and airway associated interstitial macrophages (NAMs) for disease tolerance during lethal respiratory viral infection.Research square · 2026Article
- Single-cell dissection of avian (chicken) H1N1 influenza virus coinfection dynamics in mammalian (mouse) and avian (chicken) hosts.Acta biochimica et biophysica Sinica · 2025Article
- Targeting a macrophage stemness factor to mitigate diseases post respiratory viral infection.bioRxiv : the preprint server for biology · 2025Article
- The Regulatory Network of Transcription Factors in Macrophage Polarization.ImmunoTargets and therapy · 2025Review
- The protein disulfide isomerase A3 and osteopontin axis promotes influenza-induced lung remodelling.British journal of pharmacology · 2024Article
- The Versatile Role of Peroxisome Proliferator-Activated Receptors in Immune-Mediated Intestinal Diseases.Cells · 2024Review
- Comparative single-cell analysis reveals IFN-γ as a driver of respiratory sequelae after acute COVID-19.Science translational medicine · 2024Article
- Biomaterial-mediated intracellular control of macrophages for cell therapy in pro-inflammatory and pro-fibrotic conditions.Biomaterials · 2024Article
- Changes in DNA Methylation and mRNA Expression in Lung Tissue after Long-Term Supplementation with an Increased Dose of Cholecalciferol.International journal of molecular sciences · 2023Article
- Recent advances in anti-inflammatory active components and action mechanisms of natural medicines.Inflammopharmacology · 2023Review
- Interaction among inflammasome, PANoptosise, and innate immune cells in infection of influenza virus: Updated review.Immunity, inflammation and disease · 2023Review
- Tissue-resident memory T cells and lung immunopathology.Immunological reviews · 2023Review
- Peroxisome Proliferator-Activated Receptor-Targeted Therapies: Challenges upon Infectious Diseases.Cells · 2023Review
- Tocilizumab-coated solid lipid nanoparticles loaded with cannabidiol as a novel drug delivery strategy for treating COVID-19: A review.Frontiers in immunology · 2023Review
- A glimpse of the connection between PPARγ and macrophage.Frontiers in pharmacology · 2023Review
- The role of peroxisome proliferator-activated receptors in the modulation of hyperinflammation induced by SARS-CoV-2 infection: A perspective for COVID-19 therapy.Frontiers in immunology · 2023Review
- Cannabinoids as Emergent Therapy Against COVID-19.Cannabis and cannabinoid research · 2022Review
- The impact of the lung environment on macrophage development, activation and function: diversity in the face of adversity.Mucosal immunology · 2022Review
Corrections and comments
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
Abstract
Influenza virus causes a heterogeneous respiratory infectious disease ranging from self-limiting symptoms to non-resolving pathology in the lungs. Worldwide, seasonal influenza infections claim ~500,000 lives annually. Recent reports describe pathologic pulmonary sequelae that result in remodeling the architecture of lung parenchyma following respiratory infections. These dysfunctional recovery processes that disproportionately impact the elderly have been understudied. Macrophages are involved in tissue remodeling and are critical for survival of severe influenza infection. Here, we found intrinsic deficiency of the nuclear receptor PPAR-γ in myeloid cells delayed the resolution of pulmonary inflammation following influenza infection. Mice with myeloid cell-specific PPAR-γ deficiency subsequently presented with increased influenza-induced deposition of pulmonary collagen compared to control mice. This dysfunctional lung remodeling was progressive and sustained for at least 3 months following infection of mice with myeloid PPAR-γ deficiency. These progressive changes were accompanied by a pro-fibrotic gene signature from lung macrophages and preceded by deficiencies in activation of genes involved with damage repair. Importantly similar aberrant gene expression patterns were also found in a secondary analysis of a study where macrophages were isolated from patients with fibrotic interstitial lung disease. Quite unexpectedly, mice with PPAR-γ deficient macrophages were more resistant to bleomycin-induced weight loss whereas extracellular matrix deposition was unaffected compared to controls. Therefore PPAR-γ expression in macrophages may be a pathogen-specific limiter of organ recovery rather than a ubiquitous effector pathway in response to generic damage.
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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.