ArticleMucosal immunology2015
PPARγ activation following apoptotic cell instillation promotes resolution of lung inflammation and fibrosis via regulation of efferocytosis and proresolving cytokines.
Article in Mucosal immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers, 1 of them a synthesis that pooled it.
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Who cites it
91 citing papers in PubMed, 1 synthesis or guideline pooled it, 136 citations in OpenAlex.
- The molecular mechanisms of action of PPAR-γ agonists in the treatment of corneal alkali burns (Review).International journal of molecular medicine · 2016Pooled it
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- Chitinase-like proteins de-N-glycosylating CD36 modify cholesterol metabolism in atherosclerotic macrophages.Nature communications · 2026Article
- Exclusion of Notch from the contact site during efferocytosis restricts anticancer immunity.Nature immunology · 2026Article
- Modulation of immune cells and metabolic reprogramming in efferocytosis.Cell death & disease · 2026Review
- Sophoricoside enhances reparative macrophage polarization to promote cardiac repair postmyocardial infarction through PPAR-γ.Coronary artery disease · 2026Article
- The Crosstalk Between Efferocytosis and Macrophage Polarization in Diabetic Wounds: A Comprehensive Review.Journal of inflammation research · 2026Review
- Precision Glyco-Modulation of Macrophages with EF-M2 (ImmutalonVeterinary sciences · 2025Article
- αCGRP deficiency aggravates pulmonary fibrosis by promoting senescence in alveolar type 2 cells.Genes and immunity · 2025Article
- High expression of Rex-orf-I and HBZ mRNAs and bronchiectasis in lung of HTLV-1A/C infected macaques.Nature communications · 2025Article
- Caloric restriction promotes resolution of atherosclerosis in obese mice, while weight regain accelerates its progression.The Journal of clinical investigation · 2025Article
- Beyond Killing: The Overlooked Contribution of Neutrophils to Tissue Repair.International journal of molecular sciences · 2025Review
- Anti-Atherogenic Mechanisms and Therapies.Current atherosclerosis reports · 2025Review
- Geranylgeranyl diphosphate synthase deficiency impairs efferocytosis and resolution of acute lung injury.Respiratory research · 2025Article
- Fate and long-lasting therapeutic effects of mesenchymal stromal/stem-like cells: mechanistic insights.Stem cell research & therapy · 2025Review
- Article
- Identification of diagnostic hub genes related to energy metabolism in idiopathic pulmonary fibrosis.Frontiers in molecular biosciences · 2025Article
- Gas6 induces AIM to suppress acute lung injury in mice by inhibiting NLRP3 inflammasome activation and inducing autophagy.Frontiers in immunology · 2025Article
31 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Changes in macrophage phenotype have been implicated in apoptotic cell-mediated immune modulation via induction of peroxisome proliferator-activated receptor-γ (PPARγ). In this study, we characterized PPARγ induction by apoptotic cell instillation over the course of bleomycin-induced lung injury in C57BL/6 mice. Next, the role of PPARγ activation in resolving lung inflammation and fibrosis was investigated. Our data demonstrate that apoptotic cell instillation after bleomycin results in immediate and prolonged enhancement of PPARγ mRNA and protein in alveolar macrophages and lung. Moreover, PPARγ activity and expression of its target molecules, including CD36, macrophage mannose receptor, and arginase 1, were persistently enhanced following apoptotic cell instillation. Coadministration of the PPARγ antagonist, GW9662, reversed the enhanced efferocytosis, and the reduced proinflammatory cytokine expression, neutrophil recruitment, myeloperoxidase activity, hydroxyproline contents, and fibrosis markers, including type 1 collagen α2, fibronectin and α-smooth muscle actin (α-SMA), in the lung by apoptotic cell instillation. In addition, inhibition of PPARγ activity reversed the expression of transforming growth factor-β (TGF-β), interleukin (IL)-10, and hepatocyte growth factor (HGF). These findings indicate that one-time apoptotic cell instillation contributes to anti-inflammatory and antifibrotic responses via upregulation of PPARγ expression and subsequent activation, leading to regulation of efferocytosis and production of proresolving cytokines.
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