ArticleJournal of periodontology2022
Autophagy upregulates inflammatory cytokines in gingival tissue of patients with periodontitis and lipopolysaccharide-stimulated human gingival fibroblasts.
Article in Journal of periodontology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 38 citations in OpenAlex.
- Tobacco-derived particulates and the periodontal axis: Distinct cytotoxic and stress-related mechanisms in human gingival fibroblasts.Scientific reports · 2026Article
- Targeted autophagy: research progress on the regulatory potential of periodontitis prevention and treatment.Frontiers in cell and developmental biology · 2026Review
- Exosomes from LPS-pretreated BMSCs treated periodontitis via improving oxidative stress.Stem cell research & therapy · 2025Article
- A narrative review on bridging the gap between periodontitis and cardiovascular disease: exploring the cellular and molecular mechanisms of periodontitis-driven atherosclerosis.Molecular biology reports · 2025Review
- Baicalin attenuates LPS-induced periodontal inflammation response by inhibiting autophagy.BMC oral health · 2025Article
- Periodontopathogen-Related Cell Autophagy-A Double-Edged Sword.Inflammation · 2025Review
- Effect and mechanism of Sanqi () in treating periodontitis.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025Article
- Cell-Type-Specific ROS-AKT/mTOR-Autophagy Interplay-Should It Be Addressed in Periimplantitis?Diagnostics (Basel, Switzerland) · 2024Review
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- Exploration of potential shared gene signatures between periodontitis and multiple sclerosis.BMC oral health · 2024Article
- Novel Insights from Comprehensive Bioinformatics Analysis Utilizing Large-Scale Human Transcriptomes and Experimental Validation: The Role of Autophagy in Periodontitis.Journal of inflammation research · 2024Article
- CKIP-1 Promotes P. gingivalis-Induced Inflammation of Periodontal Soft Tissues by Inhibiting Autophagy.Inflammation · 2023Article
- Glucose Starvation-Caused Oxidative Stress Induces Inflammation and Autophagy in Human Gingival Fibroblasts.Antioxidants (Basel, Switzerland) · 2022Article
- Autophagy upregulates inflammatory cytokines in gingival tissue of patients with periodontitis and lipopolysaccharide-stimulated human gingival fibroblasts.Journal of periodontology · 2022Article
- Effects of Puerarin Combined with PLGA/TCP/Puerarin on Osteocalcin and Sialoprotein of Mandibular Defects.Contrast media & molecular imaging · 2022Article
- Lipopolysaccharide-Preconditioned Dental Follicle Stem Cells Derived Small Extracellular Vesicles Treating Periodontitis via Reactive Oxygen Species/Mitogen-Activated Protein Kinase Signaling-Mediated Antioxidant Effect.International journal of nanomedicine · 2022Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPeriodontitis is an inflammatory disease caused by multiple disease-associated bacterial species in periodontal tissues. Autophagy is known to modulate various inflammation-driven diseases and inflammatory responses, but the role of autophagy related to the pathogenesis of periodontitis is not fully established. We investigated whether autophagic flux regulated the expression of inflammatory cytokines in the gingiva of periodontitis patients and lipopolysaccharide (LPS)-stimulated human gingival fibroblasts (HGFs) and the underlying mechanism.
methodsThe mRNA and protein expression of proinflammatory cytokines was assessed in human gingival tissues collected from patients with periodontitis and HGFs treated with LPS. The expression of signaling molecules related to autophagy was evaluated by immunofluorescence and Western blot analyses.
resultsThe expression of interleukin (IL)-6, tumor necrosis factor-α (TNF-α), cyclooxygenase-2 (COX-2), and intercellular adhesion molecule-1 (ICAM-1) was increased in the gingival tissues of patients with periodontitis. LC3B-positive cells, a typical autophagic marker, were increased in the gingival tissues of periodontitis patients and LPS-treated HGFs. The conversion ratio of LC3-I to LC3-II was higher in the gingival tissues associated with periodontitis and LPS-treated HGFs compared to the controls. The autophagy inhibitor 3-methyladenine (3MA) significantly abrogated the LPS-sustained inflammatory effect by reducing the expression of IL-6, TNF-α, COX-2, and ICAM-1 in HGFs. The phosphorylation of protein kinase B (AKT) and protein S6K1 (S6), signals involved in the mTOR-dependent mechanism, was decreased in gingiva derived from periodontitis patients and LPS-treated HGFs.
conclusionsAutophagy augmented the production of inflammatory cytokines by mTOR inactivation via the AKT signaling pathway in the gingival tissues of patients with periodontitis and LPS-stimulated HGFs. These findings would provide a better understanding of the mechanism by which autophagy regulates the inflammatory response associated with periodontal pathogenesis.
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