ArticleAging2018
Impaired autophagic activity and ATG4B deficiency are associated with increased endoplasmic reticulum stress-induced lung injury.
Article in Aging, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Deficient autophagy in retinal ganglion cells impairs the degradation of intracellular organelles, leading to neurodegeneration.Cell death & disease · 2026Article
- Male germ cell-specific deletion ofZoological research · 2026Article
- Tunicamycin Protects against LPS-Induced Lung Injury.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Research Progress in the Molecular Mechanisms, Therapeutic Targets, and Drug Development of Idiopathic Pulmonary Fibrosis.Frontiers in pharmacology · 2022Review
- ZKSCAN3 in severe bacterial lung infection and sepsis-induced immunosuppression.Laboratory investigation; a journal of technical methods and pathology · 2021Article
- AMPK activates Parkin independent autophagy and improves post sepsis immune defense against secondary bacterial lung infections.Scientific reports · 2021Article
- Chemical activation of SAT1 corrects diet-induced metabolic syndrome.Cell death and differentiation · 2020Article
- Autophagy in chronic lung disease.Progress in molecular biology and translational science · 2020Review
- Epithelial Injury and Dysfunction in the Pathogenesis of Idiopathic PulmonaryFibrosis.The American journal of the medical sciences · 2019Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aging is the main risk factor for the development of idiopathic pulmonary fibrosis (IPF), a progressive and usually lethal lung disorder. Although the pathogenic mechanisms are uncertain, endoplasmic reticulum (ER) stress and impaired proteostasis that have been linked with aging are strongly associated with the pathogenesis of IPF. Using the Atg4b-deficient mice as a model, that partially reproduces the autophagy deficient conditions reported in aging and IPF lungs, we show for the first time how autophagy impairment and ER stress induction, contribute simultaneously to development of lung fibrosis in vivo. Increased expression of ER stress markers, inflammation and apoptosis of alveolar epithelial cells were observed in Atg4b-deficient mice compared to WT mice, when treated with the ER stress inducer tunicamycin. After tunicamycin treatment, Atg4b null lungs showed accumulation of its substrate LC3-I, demonstrating that these mice failed to induce autophagy despite the ER stress conditions. We also showed that compromised autophagy in lungs from Atg4b null mice is associated with exacerbated lung damage, epithelial apoptosis and the development of lung fibrosis at 21 days after tunicamycin treatment. Our findings indicate that ATG4B protein and autophagy are essential to mitigate ER stress and to prevent tunicamycin-induced epithelial apoptosis and lung fibrosis.
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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.