ArticleOxidative medicine and cellular longevity2020
Sirtuin 3 Inhibits Airway Epithelial Mitochondrial Oxidative Stress in Cigarette Smoke-Induced COPD.
Article in Oxidative medicine and cellular longevity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 43 citations in OpenAlex.
- Advances in sirtuin research in lung diseases (Review).International journal of molecular medicine · 2026Review
- Pseudoephedrine Improves Chronic Obstructive Pulmonary Disease by Regulating Airway Senescence and Mitochondrial Function through PI3K/AKT/mTOR Axis.Biomolecules & therapeutics · 2026Article
- Immune-metabolic positive feedback model in COPD: cross-mechanisms and potential intervention strategies.Frontiers in cell and developmental biology · 2026Review
- NGAL knockdown alleviated CSE-induced cellular senescence and reduced MMP2 and MMP9 expression in alveolar macrophages through the PI3K/Akt pathway.European journal of medical research · 2025Article
- Roles of SIRT3 in aging and aging-related diseases.International journal of biological sciences · 2025Review
- L-ascorbate Alleviates Chronic Obstructive Pulmonary Disease through the EGF/PI3K/AKT Signaling Axis.Current medicinal chemistry · 2025Article
- Azithromycin Mitigates Tobacco Smoke-Induced Lung Senescence by Modulating the FOXO3A/CCND1 Signaling Pathway.International journal of chronic obstructive pulmonary disease · 2025Article
- Identification and validation for biomarkers associated with mitochondrial metabolism in chronic obstructive pulmonary disease.Frontiers in medicine · 2025Article
- Modulating mitochondria with natural extract compounds: from bench to clinical therapeutic opportunities for COPD.Frontiers in pharmacology · 2025Review
- The Correlation Analysis Between m6A Methylation Modification and Ferroptosis Induced by Cigarette Smoke in Human Bronchial Epithelium.Immunity, inflammation and disease · 2024Article
- Camel milk inhibits pulmonary oxidative stress and inflammation in a rat model of COPD induced by cigarette smoke exposure.Heliyon · 2024Article
- Identification of novel biomarkers related to neutrophilic inflammation in COPD.Frontiers in immunology · 2024Article
- Honokiol ameliorates cigarette smoke-induced damage of airway epithelial cells via the SIRT3/SOD2 signalling pathway.Journal of cellular and molecular medicine · 2023Article
- LncRNA PVT1 induces apoptosis and inflammatory response of bronchial epithelial cells by regulating miR-30b-5p/BCL2L11 axis in COPD.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2023Article
- Cigarette Smoke-Induced Reactive Oxygen Species Formation: A Concise Review.Antioxidants (Basel, Switzerland) · 2023Review
- Sodium pyruvate exerts protective effects against cigarette smoke extract-induced ferroptosis in alveolar and bronchial epithelial cells through the GPX4/Nrf2 axis.Journal of inflammation (London, England) · 2023Article
- Article
- Review
- The sirtuin family in health and disease.Signal transduction and targeted therapy · 2022Review
- Roles of sirtuins in asthma.Respiratory research · 2022Review
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial damage in airway epithelial cells plays an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD). Sirtuin 3 (Sirt3) is a mitochondrial deacetylase regulating mitochondrial function, but its role in the pathogenesis of COPD is still unknown. The aim of the present study was to investigate the effect of Sirt3 on airway epithelial mitochondria in cigarette smoke-induced COPD. Our present study has shown serious airway inflammation, alveolar space enlargement, and mitochondrial damage of the airway epithelium in COPD rats. Compared to the control rats, Sirt3 protein expression was significantly decreased in the airway epithelium and lung tissue homogenate from COPD rats. In airway epithelial cells (BEAS-2B), cigarette smoke extract (CSE) treatment significantly decreased mRNA and protein expression of Sirt3 and manganese superoxide dismutase (MnSOD), as well as MnSOD activity in a concentration and time-dependent manner. Sirt3 siRNA further significantly intensified the decreases in MnSOD expression and activity and aggravated mitochondrial oxidative stress and cell injury when airway epithelial cells were treated with 7.5% CSE. In contrast, Sirt3 overexpression significantly prevented the decrease of MnSOD expression and activity and improved mitochondrial oxidative stress and cell injury in CSE-treated airway epithelial cells. These data suggest that Sirt3 inhibits airway epithelial mitochondrial oxidative stress possibly through the regulation of MnSOD, thereby contributing to the pathogenesis of COPD.
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