ArticleInternational journal of oral science2022
Interleukin-13 promotes cellular senescence through inducing mitochondrial dysfunction in IgG4-related sialadenitis.
Article in International journal of oral science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 45 citations in OpenAlex.
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- Energy Metabolic Regulatory Materials Promote Wound Healing in Senescent Environment.Progress in molecular and subcellular biology · 2026Review
- Inflammaging and Senescence-Associated Secretory Phenotype (SASP) in Psoriasis - A Narrative Review of Potential Mechanisms and Anti-Inflammaging Strategies.Psoriasis (Auckland, N.Z.) · 2026Review
- Single-cell multi-omics analysis revealed the expansion of age-associated B cells in the pancreas of type 1 autoimmune pancreatitis patients.Genome medicine · 2025Article
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- Persistent accumulation of therapy-induced senescent cells: an obstacle to long-term cancer treatment efficacy.International journal of oral science · 2025Review
- The composition of single-donor apheresis platelet concentrates is influenced by the age of the donor.Scientific reports · 2025Article
- Antioxidant Senotherapy by Natural Compounds: A Beneficial Partner in Cancer Treatment.Antioxidants (Basel, Switzerland) · 2025Review
- Modulation of STAT6 signaling for hepatoprotection.Frontiers in pharmacology · 2025Review
- Exploring the differential functions of circulating follicular helper T and peripheral helper T cells in rheumatoid arthritis based on metabolism patterns.Frontiers in immunology · 2025Article
- Identification and culture of functional salivary gland ductal epithelial cells.Histochemistry and cell biology · 2024Article
- SenMayo transcriptomic senescence panel highlights glial cells in the ageing mouse and human retina.npj aging · 2024Article
- Decoding senescence of aging single cells at the nexus of biomaterials, microfluidics, and spatial omics.npj aging · 2024Review
- LRRC8A drives NADPH oxidase-mediated mitochondrial dysfunction and inflammation in allergic rhinitis.Journal of translational medicine · 2024Article
- Identification of circRNAs expression profiles and functional networks in parotid gland of type 2 diabetes mouse.BMC genomics · 2024Article
- Pregnane X Receptor Activation in Liver Macrophages Protects against Endotoxin-Induced Liver Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Expression of USP25 associates with fibrosis, inflammation and metabolism changes in IgG4-related disease.Nature communications · 2024Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immunoglobulin G4-related sialadenitis (IgG4-RS) is an immune-mediated fibro-inflammatory disease and the pathogenesis is still not fully understood. The aim of this study was to explore the role and mechanism of interleukin-13 (IL-13) in the cellular senescence during the progress of IgG4-RS. We found that the expression of IL-13 and IL-13 receptor α1 (IL-13Rα1) as well as the number of senescent cells were significantly higher in the submandibular glands (SMGs) of IgG4-RS patients. IL-13 directly induced senescence as shown by the elevated activity of senescence-associated β-galactosidase (SA-β-gal), the decreased cell proliferation, and the upregulation of senescence markers (p53 and p16) and senescence-associated secretory phenotype (SASP) factors (IL-1β and IL-6) in SMG-C6 cells. Mechanistically, IL-13 increased the level of phosphorylated signal transducer and activator of transcription 6 (p-STAT6) and mitochondrial-reactive oxygen species (mtROS), while decreased the mitochondrial membrane potential, ATP level, and the expression and activity of superoxide dismutase 2 (SOD2). Notably, the IL-13-induced cellular senescence and mitochondrial dysfunction could be inhibited by pretreatment with either STAT6 inhibitor AS1517499 or mitochondria-targeted ROS scavenger MitoTEMPO. Moreover, IL-13 increased the interaction between p-STAT6 and cAMP-response element binding protein (CREB)-binding protein (CBP) and decreased the transcriptional activity of CREB on SOD2. Taken together, our findings revealed a critical role of IL-13 in the induction of salivary gland epithelial cell senescence through the elevated mitochondrial oxidative stress in a STAT6-CREB-SOD2-dependent pathway in IgG4-RS.
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