ArticleAntioxidants (Basel, Switzerland)2022
Glucose Starvation-Caused Oxidative Stress Induces Inflammation and Autophagy in Human Gingival Fibroblasts.
Article in Antioxidants (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Energy Metabolic Regulatory Materials Promote Wound Healing in Senescent Environment.Progress in molecular and subcellular biology · 2026Review
- Integrated bioinformatics analysis identifies glutathione metabolism-related genes as diagnostic biomarkers for periodontitis.BMC oral health · 2025Article
- Involvement of oxidative stress in orofacial mechanical pain hypersensitivity following neonatal maternal separation in rats.Scientific reports · 2023Article
- Article
- Essential Amino Acid Starvation-Induced Oxidative Stress Causes DNA Damage and Apoptosis in Murine Osteoblast-like Cells.International journal of molecular sciences · 2023Article
- Photodynamic reactions using high-intensity red LED promotes gingival wound healing by ROS induction.Scientific reports · 2023Article
- SIRT3/GLUT4 signaling activation by metformin protect against cisplatin-induced ototoxicity in vitro.Archives of toxicology · 2023Article
- An engineered biomaterial to harness the differentiation potential of endogenous human gingival mesenchymal stem cells (hGMSCs).Frontiers in dental medicine · 2023Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Gingival tissue experiences an environment of nutrient shortage, such as low glucose conditions, after periodontal surgery. Our previous studies found that this low glucose condition inhibits normal gingival cell functions. However, the mechanism by which this glucose-deficient environment causes cellular damage to human gingival fibroblasts (HGnFs) remains unclear. This study aimed to investigate the biological effects of ROS induction on HGnFs under low glucose conditions. ROS levels and cellular anti-ROS ability of HGnFs under different glucose concentrations were evaluated by measuring ROS formation and the expression of superoxide dismutase and heme oxygenase 1. Changes in cellular viability were investigated using 5-bromo-2'-deoxyuridine assay and cell survival detection, and the cellular damage was evaluated by the expression of inflammatory cytokines and changes in the expression of autophagy-related protein. ROS formation was then blocked using N-acetyl-L-cysteine (NAC), and the effects of ROS on HGnFs under low glucose conditions were investigated. Low glucose conditions induced ROS accumulation, reduced cellular activity, and induced inflammation and autophagy. After NAC application, the anti-ROS capacity increased, cellular activity improved, and inflammation and autophagy were controlled. This can be effectively controlled by the application of antioxidants such as NAC.
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Registered trials
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.