ArticleInternational journal of molecular sciences2020
Modulation of NLRP3 Inflammasome through Formyl Peptide Receptor 1 (Fpr-1) Pathway as a New Therapeutic Target in Bronchiolitis Obliterans Syndrome.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 82 citations in OpenAlex.
- Monocolonization withMicrobiology spectrum · 2026Article
- Protective Effects of Cyclosporin H Against Sepsis-Induced Acute Kidney Injury via Modulation of Fpr1 Signaling and Inhibiting Pyroptosis.Research and reports in urology · 2026Article
- Mesenchymal stromal cell extracellular vesicles reduceAmerican journal of physiology. Lung cellular and molecular physiology · 2025Article
- Let-7b-5p loaded Mesenchymal Stromal Cell Extracellular Vesicles reducebioRxiv : the preprint server for biology · 2025Article
- CIP2A promotes bronchiolitis obliterans by activating the NF‑κB pathway.Molecular medicine reports · 2025Article
- Iron Overload-induced Ferroptosis as a Target for Protection against Obliterative Bronchiolitis after Orthotopic Tracheal Transplantation in Mice.Current molecular medicine · 2025Article
- A Novel Compound Ligusticum Cycloprolactam Alleviates Neuroinflammation After Ischemic Stroke via the FPR1/NLRP3 Signaling Axis.CNS neuroscience & therapeutics · 2024Article
- NLRP3 Inflammasome Involvement in Heart, Liver, and Lung Diseases-A Lesson from Cytokine Storm Syndrome.International journal of molecular sciences · 2023Review
- Transcriptome analysis reveals the impact of NETs activation on airway epithelial cell EMT and inflammation in bronchiolitis obliterans.Scientific reports · 2023Article
- Antioxidant Activity of a Sicilian Almond Skin Extract Using In Vitro and In Vivo Models.International journal of molecular sciences · 2023Article
- Fisetin, a Natural Polyphenol, Ameliorates Endometriosis Modulating Mast Cells Derived NLRP-3 Inflammasome Pathway and Oxidative Stress.International journal of molecular sciences · 2023Article
- The Role of the NLRP3 Inflammasome and Programmed Cell Death in Acute Liver Injury.International journal of molecular sciences · 2023Review
- Formyl peptide receptor-1 (FPR1) represses intestinal oncogenesis.Oncoimmunology · 2023Article
- Rs867228 in FPR1 accelerates the manifestation of luminal B breast cancer.Oncoimmunology · 2023Article
- Regulation of Apoptosis and Oxidative Stress by Oral Boswellia Serrata Gum Resin Extract in a Rat Model of Endometriosis.International journal of molecular sciences · 2022Article
- Açai Berry Attenuates Cyclophosphamide-Induced Damage in Genitourinary Axis-Modulating Nrf-2/HO-1 Pathways.Antioxidants (Basel, Switzerland) · 2022Article
- Review
- Açai Berry Mitigates Parkinson's Disease Progression Showing Dopaminergic Neuroprotection via Nrf2-HO1 Pathways.Molecular neurobiology · 2022Article
- Chronic Exposure to Endocrine Disruptor Vinclozolin Leads to Lung Damage via Nrf2-Nf-kb Pathway Alterations.International journal of molecular sciences · 2022Article
- Chronic Exposure to Vinclozolin Induced Fibrosis, Mitochondrial Dysfunction, Oxidative Stress, and Apoptosis in Mice Kidney.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic rejection is the major leading cause of morbidity and mortality after lung transplantation. Bronchiolitis obliterans syndrome (BOS), a fibroproliferative disorder of the small airways, is the main manifestation of chronic lung allograft rejection. We investigated, using transgenic mice, the mechanisms through which the deficiency of IL-1β/IL-18, Casp-1, or Fpr-1 genes could be protective in an experimental model of BOS, induced in mice by allogeneic heterotopic tracheal transplantation. Fpr-1 KO mice showed a marked reduction in histological markers of BOS and of mast cell numbers compared to other groups. Molecular analyses indicated that the absence of the Fpr-1 gene was able to decrease NF-κB nuclear translocation and modulate NLRP3 inflammasome signaling and the mitogen-activated protein kinase (MAPK) pathway in a more significant way compared to other groups. Additionally, Fpr-1 gene deletion caused a reduction in resistance to the apoptosis, assessed by the TUNEL assay. Immunohistochemical analyses indicated changes in nitrotyrosine, PARP, VEGF, and TGF-β expression associated with the pathology, which were reduced in the absence of the Fpr1 gene more so than by the deletion of IL-1β/IL-18 and Casp-1. We underline the importance of the NLRP3 inflammasome and the pathogenic role of Fpr-1 in experimental models of BOS, which is the result of the modulation of immune cell recruitment together with the modulation of local cellular activation, suggesting this gene as a new target in the control of the pathologic features of BOS.
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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.