ArticleLaboratory investigation; a journal of technical methods and pathology2019
Lipopolysaccharide promotes lung fibroblast proliferation through autophagy inhibition via activation of the PI3K-Akt-mTOR pathway.
Article in Laboratory investigation; a journal of technical methods and pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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32 citing papers in PubMed, 48 citations in OpenAlex.
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- One-Stone-Three-Birds Biomimetic Oral Targeting Delivery Strategy for On-Demand Controlled Drug Release and Intervertebral Disc Degeneration Therapy.Exploration (Beijing, China) · 2026Article
- EV-associated non-coding RNAs in paediatric asthma airway remodelling: current mechanistic evidence and therapeutic perspectives.Frontiers in pharmacology · 2026Review
- Endocan attenuates LPS-induced alveolar type II cells injury through PI3K/Akt/mTOR pathway.Upsala journal of medical sciences · 2026Article
- Lipopolysaccharide-induced histone lactylation mediates m6A RNA modification causing mitochondrial dysfunction and pulmonary fibroblasts activation to exacerbate sepsis-associated pulmonary fibrosis.Respiratory research · 2025Article
- Mitomycin C Induces Autophagy in Human Tracheal Fibroblasts and Suppresses Their Growth.Laryngoscope investigative otolaryngology · 2025Article
- The therapeutic effect of Qishen Huoxue Granule on myocardial injury in sepsis rats and its underlying mechanism via suppressing excessive autophagy.Scientific reports · 2025Article
- IL-17A regulates airway remodelling in COPD through the PI3K/AKT/mTOR pathway.Scientific reports · 2025Article
- PGC-1α mediates migrasome secretion accelerating macrophage-myofibroblast transition and contributing to sepsis-associated pulmonary fibrosis.Experimental & molecular medicine · 2025Article
- Fibroblast PI3K/AKT signaling and extracellular matrix homeostasis: mechanisms, targets, and delivery challenges.Frontiers in cell and developmental biology · 2025Review
- PI3K/Akt in IPF: untangling fibrosis and charting therapies.Frontiers in immunology · 2025Review
- Modulation of gut microbiota in targeted cancer therapy: insights on the EGFR/VEGF/KRAS pathways.Cancer biology & medicine · 2024Review
- Sodium propionate ameliorates lipopolysaccharide-induced acute respiratory distress syndrome in rats via the PI3K/AKT/mTOR signaling pathway.3 Biotech · 2024Article
- The role of autophagy regulated by the PI3K/AKT/mTOR pathway and innate lymphoid cells in eosinophilic chronic sinusitis with nasal polyps.Immunity, inflammation and disease · 2024Article
- The impact of glucose metabolism on inflammatory processes in sepsis-induced acute lung injury.Frontiers in immunology · 2024Review
- Article
- Cellular and Molecular Mechanisms in Idiopathic Pulmonary Fibrosis.Advances in respiratory medicine · 2023Review
- Autophagy in pulmonary fibrosis: friend or foe?Genes & diseases · 2022Article
- Integrative immunogenomic analysis reveals transcriptional and immune-related differences in hepatocellular carcinoma patients with different disease-free survival.American journal of cancer research · 2022Article
- Identifying the molecular targets and mechanisms of xuebijing injection for the treatment of COVID-19 via network parmacology and molecular docking.Bioengineered · 2021Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pulmonary fibrosis is a major cause of death in patients with acute respiratory distress syndrome (ARDS). Our previous study revealed that lipopolysaccharide (LPS) challenge could lead to mouse lung fibroblast proliferation. Additionally, inhibition of autophagy in lung fibroblasts was also reported to be crucial during the process of pulmonary fibrosis. However, the correlation between proliferation and inhibition of autophagy of lung fibroblasts and the underlying mechanism remain unknown. In this study, we report that autophagy was inhibited in mouse lung fibroblasts after LPS challenge, and was accompanied by activation of the PI3K-Akt-mTOR signaling pathway. Treating mouse lung fibroblasts with LPS resulted in mTOR and Akt phosphorylation, p62 up-regulation, and significant down-regulation of autophagosomes, which could be reversed by PI3K-Akt inhibitors (Ly294002) or mTOR inhibitors (rapamycin, RAPA). Furthermore, either LPS or hydroxychloroquine (HCQ), an autophagy inhibitor, could promote mouse lung fibroblast proliferation, which could be reversed by RAPA application. The present research therefore reveals that LPS promotes lung fibroblast proliferation through autophagy inhibition via activation of the PI3K-Akt-mTOR pathway.
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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.