ArticleInternational journal of biological sciences2024
SGK1 aggravates idiopathic pulmonary fibrosis by triggering H3k27ac-mediated macrophage reprogramming and disturbing immune homeostasis.
Article in International journal of biological sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 21 citations in OpenAlex.
- Interaction between ZMIZ2 and AR promotes prostate cancer proliferation in vitro and in vivo.Cancer biology & therapy · 2026Article
- A drug-repurposing nanotheranostic for synergistic management of resistant bacterial pneumonia.Asian journal of pharmaceutical sciences · 2026Article
- The β-hydroxybutyrylation of Zyxin ameliorates pulmonary fibrosis by inhibiting lung fibroblast activation through the PI3K/AKT pathway.Respiratory research · 2026Article
- Exploring the role of RCEO in macrophage-mediated modulation of pulmonary fibrosis.Chinese medicine · 2026Article
- Research on Therapeutic Strategy of Inhalable Cell Membrane-Coated Nanodelivery Complexes Mediating Nrf2 Pathway for Ameliorating Pulmonary Fibrosis.ACS applied materials & interfaces · 2026Article
- Profibrotic macrophage populations and cell communications in pulmonary fibrosis.Journal of physiology and biochemistry · 2026Review
- Prognostic Significance of SGK1 Expression in Multiple Myeloma Patients Undergoing Autologous Hematopoietic Stem Cell Transplantation: A Single-Center Retrospective Study.Stem cells international · 2026Article
- The gene regulatory networks shaping macrophage plasticity and altered function in fibrosis.Frontiers in immunology · 2026Review
- Antifibrotic Strategies Targeting Phosphodiesterase-4 in Idiopathic Pulmonary Fibrosis: Molecular Mechanisms and Clinical Translation.Clinical pharmacology : advances and applications · 2026Review
- Variable steady inflammation and inflammatory responses in precision-cut lung slices from various IPF lung Regions.Respiratory research · 2025Article
- Molecular mechanisms of efferocytosis imbalance in the idiopathic pulmonary fibrosis microenvironment: from gene screening to dynamic regulation analysis.Biology direct · 2025Article
- Therapeutic targeting of myeloid cells in liver fibrosis: Mechanisms and clinical prospects.Animal models and experimental medicine · 2025Review
- NADAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Neutrophils as key drivers of pulmonary fibrosis: unveiling mechanisms and therapeutic implications.Frontiers in immunology · 2025Review
- Diabetes mellitus-driven pulmonary injury: multidimensional mechanisms linking metabolic dysregulation to gut-lung axis and promising therapies.Frontiers in pharmacology · 2025Review
- Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic pulmonary fibrosis (IPF) is characterized by fibrotic matrix deposition and irreversible aberrant tissue remodeling. Their mechanisms of action are associated with the activation of macrophages and a disturbed immune environment. We aim to determine how these activated macrophages influenced the pathogenesis of pulmonary fibrosis. We found the fibrotic areas of IPF patients contained more serum and glucocorticoid-induced kinase 1 (SGK1)-positive and M2-type macrophages. Similarly, bleomycin (BLM)+LPS significantly triggered high expression of SGK1 in the IPF mice, accompanied by destroyed lung structure and function, increased fibrosis markers and disturbed immune microenvironment. Mechanistically, SGK1 markedly promoted the reprogramming of M2-type macrophages in fibrotic lungs by triggering glycogen synthase kinase 3beta (GSK3β)-tat-interacting protein 60 (TIP60)- histone-3 lysine-27 acetylation (H3K27ac) signalings, which further released chemokine (C-C motif) ligand 9 (CCL9) to attract Th17 cells and delivered TGF-β to fibroblasts for synergistically destroying immune microenvironment, which was largely reversed by macrophage depletion in mice. We took macrophages as the entry point to deeply analyze IPF pathogenesis and further provided insights for the development of novel drugs represented by SGK1.
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Registered trials
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