ArticleMolecular medicine reports2015
Particulate matter 2.5 induces autophagy via inhibition of the phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin kinase signaling pathway in human bronchial epithelial cells.
Article in Molecular medicine reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 54 citations in OpenAlex.
- The triple-hit hypothesis: exploring pulmonary e-cigarette, PMEuropean respiratory review : an official journal of the European Respiratory Society · 2026Review
- Autophagy and Respiratory Viruses: Mechanisms, Viral Exploitation, and Therapeutic Insights.Cells · 2025Review
- Human Monocyte-Derived Macrophages Demonstrate Distinct Responses to Ambient Particulate Matter in a Polarization State- and Particle Seasonality-Specific Manner.Chemical research in toxicology · 2025Article
- Capsaicin Attenuates LPS-Induced Acute Lung Injury by Inhibiting Inflammation and Autophagy Through Regulation of the TRPV1/AKT Pathway.Journal of inflammation research · 2024Article
- The Road to Malignant Cell Transformation after Particulate Matter Exposure: From Oxidative Stress to Genotoxicity.International journal of molecular sciences · 2023Review
- Irisin Ameliorates PM2.5-Induced Acute Lung Injury by Regulation of Autophagy Through AMPK/mTOR Pathway.Journal of inflammation research · 2023Article
- Effects of Antioxidant on Oxidative Stress and Autophagy in Bronchial Epithelial Cells Exposed to Particulate Matter and Cigarette Smoke Extract.Tuberculosis and respiratory diseases · 2022Article
- Damage to Olfactory Organs of Adult Zebrafish Induced by Diesel Particulate Matter.International journal of molecular sciences · 2021Article
- Airway hyperresponsiveness development and the toxicity of PM2.5.Environmental science and pollution research international · 2021Review
- IL-17A-producing T cells exacerbate fine particulate matter-induced lung inflammation and fibrosis by inhibiting PI3K/Akt/mTOR-mediated autophagy.Journal of cellular and molecular medicine · 2020Article
- Inactivation of MTOR promotes autophagy-mediated epithelial injury in particulate matter-induced airway inflammation.Autophagy · 2020Article
- Deciphering the Code between Air Pollution and Disease: The Effect of Particulate Matter on Cancer Hallmarks.International journal of molecular sciences · 2019Review
- Environmental Exposures and Asthma Development: Autophagy, Mitophagy, and Cellular Senescence.Frontiers in immunology · 2019Review
- In Vitro and In Vivo Experimental Studies of PMInternational journal of environmental research and public health · 2018Review
- Function of PM2.5 in the pathogenesis of lung cancer and chronic airway inflammatory diseases.Oncology letters · 2018Review
- A Review of Recent Advances in Research on PMInternational journal of environmental research and public health · 2018Review
- [Protective effect of paeoniflorin against PM2.5-induced damage in BEAS-2B cells].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2018Article
- Repeated PM2.5 exposure inhibits BEAS-2B cell P53 expression through ROS-Akt-DNMT3B pathway-mediated promoter hypermethylation.Oncotarget · 2016Article
- Soft TCPTP Agonism-Novel Target to Rescue Airway Epithelial Integrity by Exogenous Spermidine.Frontiers in pharmacology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
Abstract
Particulate matter 2.5 (PM2.5) is a significant risk factor for asthma. A recent study revealed that autophagy was associated with asthma pathogenesis. However, the specific mechanisms underlying PM2.5-induced autophagy in asthma have remained elusive. In the present study, PM2.5-induced autophagy was evaluated in Beas-2B human bronchial epithelial cells and the potential molecular mechanisms were investigated. Using electron microscopy, immunofluorescence staining and immunoblot studies, it was confirmed that PM2.5 induced autophagy in Beas-2B cells as a result of PM2.5-mediated inhibition of the phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway in Beas-2B cells. LY294002, a PI3K inhibitor, reduced the accumulation of microtubule-associated protein 1 light chain 3 II and attenuated the effect of PM2.5. Phosphorylated (p-)p38, p-extracellular signal-regulated kinase and p-c-Jun N-terminal kinase were dephosphorylated following exposure to PM2.5. The roles of p53, reactive oxygen species scavenger tetramethylthiourea and autophagy inhibitor 3-methyladenine in PM2.5-induced autophagy in Beas-2B cells were also investigated. The results suggested that the PI3K/Akt/mTOR signaling pathway may be a key contributor to PM2.5-induced autophagy in Beas-2B cells. The results of the present study therefore provided an a insight into potential future clinical applications targeting these signaling pathways, for the prevention and/or treatment of PM2.5-induced lung diseases.
Indexed as
Identifiers
What OpenQuestion holds
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.