ArticleCell death & disease2019
Autophagic flux blockage in alveolar epithelial cells is essential in silica nanoparticle-induced pulmonary fibrosis.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 95 citations in OpenAlex.
- Organelle Crosstalk and Metabolic Reprogramming in Idiopathic Pulmonary Fibrosis: Mechanisms and Therapeutic Implications.Cell biochemistry and function · 2026Review
- Targeted lysosomal activation in bladder epithelium enhances clearance of intracellular uropathogenic Escherichia coli.PLoS pathogens · 2026Article
- Deciphering Pathogenesis of Silica Nanoparticle-Induced Airway Remodeling and Fibrosis: Insights from a Human Patient Cohort and a Murine Model.Nanomaterials (Basel, Switzerland) · 2026Article
- Targeting the senescence‒autophagy axis via p16Signal transduction and targeted therapy · 2026Article
- Integration of bioinformatics analysis and experimental verification reveals the role of neutrophil extracellular traps in silica nanoparticles-induced lung injury.Journal of nanobiotechnology · 2026Article
- Article
- House dust mite-induced autophagy dysregulation and apoptosis in bronchial epithelial injury in asthma.Frontiers in pediatrics · 2026Article
- Long-term SiNPs exposure induced genetic instability and malignant transformation via SQSTM1/p62-mediated autophagy dysfunction in lungs.Materials today. Bio · 2025Article
- Autophagy and exosome dynamics in Radiation-Induced pulmonary fibrosis: the critical role of TRIB3.Respiratory research · 2025Article
- Toxicity study of silica nanoparticles following 94-day repeated oral administration in Sprague Dawley rats.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- 2-dodecyl-6-methoxycyclohexa-2,5-diene-1,4-dione mediates the effect of ROS-enhanced PI3K/Akt/mTOR pathway on autophagy in breast cancer.FEBS open bio · 2025Article
- Current Understanding of Pulmonary Fibrosis: Pathogenesis, Diagnosis, and Therapeutic Approaches.Canadian respiratory journal · 2025Review
- Lung Single-Cell Transcriptomics Offers Insights into the Pulmonary Interstitial Toxicity Caused by Silica Nanoparticles.Environment & health (Washington, D.C.) · 2024Article
- Epithelium-derived exosomes promote silica nanoparticles-induced pulmonary fibroblast activation and collagen deposition via modulating fibrotic signaling pathways and their epigenetic regulations.Journal of nanobiotechnology · 2024Article
- Pazopanib attenuated bleomycin-induced pulmonary fibrosis via suppressing TGF-β1 signaling pathway.Journal of thoracic disease · 2024Article
- The impact of nanomaterials on autophagy across health and disease conditions.Cellular and molecular life sciences : CMLS · 2024Review
- C5a/C5aR1 axis as a key driver promotes epithelial-to-mesenchymal transition in airway epithelial cells in silica nanoparticles-induced pulmonary fibrosis.International immunopharmacology · 2023Article
- Bioactive silica nanoparticles target autophagy, NF-κB, and MAPK pathways to inhibit osteoclastogenesis.Biomaterials · 2023Article
- Kinetics of autophagic activity in nanoparticle-exposed lung adenocarcinoma (A549) cells.Autophagy reports · 2023Article
- Recent advances in nanoparticle applications in respiratory disorders: a review.Frontiers in pharmacology · 2023Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Silica nanoparticles (SiNPs) have been reported to induce pulmonary fibrosis (PF) with an unknown mechanism. Recently, the activation of autophagy, a lysosome-dependent cell degradation pathway, by SiNPs has been identified in alveolar epithelial cells (AECs). However, the underlying mechanism and the relevance of SiNPs-induced autophagy to the development of PF remain elusive. Here, we report that autophagy dysfunction and subsequent apoptosis in AECs are involved in SiNPs-induced PF. SiNPs engulfed by AECs enhance autophagosome accumulation and apoptosis both in vivo and in vitro. Mechanically, SiNPs block autophagy flux through impairing lysosomal degradation via acidification inhibition. Lysosomal reacidification by cyclic-3',5'-adenosine monophosphate (cAMP) significantly enhances autophagic degradation and attenuate apoptosis. Importantly, enhancement of autophagic degradation by rapamycin protects AECs from apoptosis and attenuates SiNPs-induced PF in the mouse model. Altogether, our data demonstrate a repressive effect of SiNPs on lysosomal acidification, contributing to the decreased autophagic degradation in AECs, thus leading to apoptosis and subsequent PF. These findings may provide an improved understanding of SiNPs-induced PF and molecular targets to antagonize it.
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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.