ArticleExperimental and therapeutic medicine2021
PM2.5 induces autophagy-mediated cell apoptosis via PI3K/AKT/mTOR signaling pathway in mice bronchial epithelium cells.
Article in Experimental and therapeutic medicine, 2021. 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, 22 citations in OpenAlex.
- Exploring the immunomodulatory effects of environmental contaminants on autoimmune patients: AnJournal of translational autoimmunity · 2026Article
- Health Risk and Pathogenesis of PMToxics · 2026Review
- Molecular mechanisms of air pollution-induced carcinogenesis and the emerging role of microplastics.Human genomics · 2025Review
- Long-Term Ambient Air Pollution Exposure and the Risk of Cardiovascular and Cerebrovascular Diseases in Rural Chinese Populations: 10-Year Follow-Up of a Multicenter Prospective Cohort Study.JMIR public health and surveillance · 2025Article
- The Associations of Air Pollution Mixture Exposure with Plasma Proteins in an Elderly U.S. Panel.Environmental science & technology · 2025Article
- Impact of Particulate Matter 2.5 on Neurological Diseases: Insights Into Pathophysiological and Molecular Mechanisms.Journal of toxicology · 2025Review
- Hyperoxia can Induce Lung Injury by Upregulating AECII Autophagy and Apoptosis Via the mTOR Pathway.Molecular biotechnology · 2024Article
- Recent advances in the epithelial barrier theory.International immunology · 2024Review
- Effect of altered human exposome on the skin and mucosal epithelial barrier integrity.Tissue barriers · 2023Article
- 3-Bromo-4,5-dihydroxybenzaldehyde Protects Keratinocytes from Particulate Matter 2.5-Induced Damages.Antioxidants (Basel, Switzerland) · 2023Article
- The Road to Malignant Cell Transformation after Particulate Matter Exposure: From Oxidative Stress to Genotoxicity.International journal of molecular sciences · 2023Review
- Apoptotic volume decrease (AVD) in AFrontiers in physiology · 2023Article
- Effect of Acute PM2.5 Exposure on Lung Function in Children: A Systematic Review and Meta-Analysis.Journal of asthma and allergy · 2023Article
- Fine Particulate Matter Exposure Levels in Patients with Normal-Tension Glaucoma and Primary Open-Angle Glaucoma: A Population-Based Study from Taiwan.International journal of environmental research and public health · 2022Article
- D-tagatose protects against oleic acid-induced acute respiratory distress syndrome in rats by activating PTEN/PI3K/AKT pathway.Frontiers in immunology · 2022Article
- Accelerated Aging and Age-Related Diseases (CVD and Neurological) Due to Air Pollution and Traffic Noise Exposure.International journal of molecular sciences · 2021Review
- Effect of Aerobic Exercise on Oxidative Stress and Inflammatory Response During Particulate Matter Exposure in Mouse Lungs.Frontiers in physiology · 2021Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Air pollution can highly impact the respiratory system in healthy individuals. Studies have indicated that particles with an aerodynamic diameter of ≤2.5 µm (PM2.5) can be considered to be harmful for lung alveoli and bronchial epithelium cells. PM2.5 can be directly inhaled and can deeply penetrate into the lung alveoli, causing lung dysfunction. However, the toxicological mechanism mediated by PM2.5 for respiratory disease has still not been clearly determined. The purpose of the current study was to investigate the effects of PM2.5 on mouse bronchial epithelium cells (MBECs) and explored the possible mechanism mediated by PM2.5 in MBECs. The results of the current study indicated that PM2.5 markedly decreased lung function, including total lung capacity, residual volume, vital capacity and airway resistance in experimental mice. The results demonstrated that PM2.5 markedly induced inflammatory responses, oxidative injury and MBEC apoptosis. PM2.5 increased interleukin (IL)-1β and IL-6 expression, and reactive oxygen species production in MBECs. Furthermore, PM2.5 specifically induced PI3K, AKT and mTOR expression in MBECs. Disruption of PI3K/AKT/mTOR signaling was also indicated to effectively inhibit apoptosis of MBECs. In conclusion, the results of the current study systematically demonstrated the role of apoptosis-mediated MBEC apoptosis in PM2.5-treated mice, and provides a potential strategy for preclinical intervention in patients with PM2.5-induced lung diseases.
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