ArticleJournal of immunology research2022
The Roles of Autophagy, Mitophagy, and the Akt/mTOR Pathway in the Pathogenesis of Chronic Rhinosinusitis with Nasal Polyps.
Article in Journal of immunology research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 17 citations in OpenAlex.
- RNA binding protein ZFP36L1 promotes ferroptosis in chronic rhinosinusitis by destabilizing CAMK2A mRNA and impairing mitochondrial quality control.Clinical and translational medicine · 2026Article
- Tacrolimus inhibits CVB3-targeted regulation of TFEB by PPP3/calcineurin.Frontiers in cellular and infection microbiology · 2026Article
- HMGB1 impairs nasal mucosa epithelial barrier function in allergic rhinitis by promoting BECN1-mediating autophagy.Biochemistry and biophysics reports · 2025Article
- Double-edged mitophagy: balancing inflammation and resolution in lung disease.Clinical science (London, England : 1979) · 2025Review
- Exploring the Causal Role of miR-941 in Chronic Rhinosinusitis: Insights from Transcriptomics and Genomics.International journal of general medicine · 2025Article
- Identification and validation of autophagy-related genes and exploration of their relationship with disease severity in chronic rhinosinusitis with nasal polyps.Asia Pacific allergy · 2024Article
- Integrated machine learning and bioinformatic analysis of mitochondrial-related signature in chronic rhinosinusitis with nasal polyps.The World Allergy Organization journal · 2024Article
- Role of autophagy and mitophagy of group 2 innate lymphoid cells in allergic and local allergic rhinitis.The World Allergy Organization journal · 2024Article
- Autophagy in chronic rhinosinusitis with or without nasal polyps.Frontiers in cell and developmental biology · 2024Review
- Serum Proteomic Analysis Revealed Biomarkers for Eosinophilic Chronic Rhinosinusitis with Nasal Polyps Pathophysiology.Journal of inflammation research · 2024Article
- TFE3 and TP53 were novel diagnostic biomarkers related to mitochondrial autophagy in chronic rhinosinusitis with nasal polyps.Frontiers in genetics · 2024Article
- Increased epithelial mTORC1 activity in chronic rhinosinusitis with nasal polyps.bioRxiv : the preprint server for biology · 2023Article
- Comprehensive analysis of mitophagy-related genes in diagnosis and heterogeneous endothelial cells in chronic rhinosinusitis: based on bulk and single-cell RNA sequencing data.Frontiers in genetics · 2023Article
- Pathogenesis and treatment of chronic rhinosinusitis from the perspective of sinonasal epithelial dysfunction.Frontiers in medicine · 2023Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathogenesis of CRSwNP is complex and unclear. CRSwNP is subdivided into two types based on the infiltration of EOSs: eCRSwNP and noeCRSwNP. This study was designed to seek the role of autophagy, mitophagy, and Akt/mTOR pathway in these two subtypes of CRSwNP. This study included 29 patients with CRSwNP and 9 controls. The levels of autophagy, mitophagy, and Akt/mTOR pathway-related proteins in nasal tissues were quantified using western blot analysis. Levels of eosinophilic inflammation-related cytokines in nasal tissues were quantified by enzyme-linked immunosorbent assay. Immunohistochemistry was also used to evaluate autophagy, mitophagy, and Akt/mTOR pathway-related protein expression and distribution in nasal polyps and control tissues. Transmission electron microscopy was used to detect the formation of autophagosomes and mitochondrial autophagosomes. Masson's trichrome and periodic acid-Schiff Alcian blue staining were used to evaluate the severity of tissue remodeling. The expression of p-Akt/Akt and p-mTOR/mTOR was upregulated in patients with eCRSwNP or noeCRSwNP. Beclin 1, PINK1, BNIP3, and FUNDC1 levels were significantly reduced in the nasal polyps of patients with eCRSwNP or noeCRSwNP. Autophagosomes and mitochondrial autophagosomes formed less frequently in the nasal polyps of patients with eCRSwNP or noeCRSwNP. Levels of IL-4, IL-5, IL-13, and ECP and the eotaxins CCL11, CCL24, and CCL26 were elevated in the nasal polyps of patients with eCRSwNP or noeCRSwNP. Tissue remodeling is enhanced in patients with eCRSwNP or noeCRSwNP. The Akt/mTOR pathway, eosinophilic inflammation, and tissue remodeling are activated in the nasal polyps of patients with eCRSwNP or noeCRSwNP. The downregulation of autophagy and mitophagy is also observed in eosinophilic and noneosinophilic nasal polyps. The targeting of mitophagy may provide new therapeutic options for different endotypes of CRSwNP.
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