ArticleAmerican journal of respiratory cell and molecular biology2012
Role of endoplasmic reticulum stress in age-related susceptibility to lung fibrosis.
Article in American journal of respiratory cell and molecular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 1 of them a synthesis that pooled it.
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.
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
75 citing papers in PubMed, 1 synthesis or guideline pooled it, 130 citations in OpenAlex.
- The Role of Herpes Viruses in Pulmonary Fibrosis.Frontiers in medicine · 2021Pooled it
- Asbestos-induced disruption of calcium homeostasis induces endoplasmic reticulum stress in macrophages.The Journal of biological chemistry · 2014Trial
- Ageing-associated regenerative failure in the lung: stem cell senescence and transitional cell persistence in idiopathic pulmonary fibrosis.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Hallmarks of the ageing lung: 10 years later.The European respiratory journal · 2026Review
- Aging and lung diseases: Unraveling mechanisms and therapeutic targets.Chinese medical journal pulmonary and critical care medicine · 2025Review
- Tissue Fibrosis Decoded via Cellular Senescence: Mechanisms, Treatments, and Emerging Technologies.Aging and disease · 2025Review
- A novel pulmonary fibrosis NOD/SCID murine model with natural aging.BMC pulmonary medicine · 2024Article
- Simvastatin attenuates silica-induced pulmonary inflammation and fibrosis in rats via the AMPK-NOX pathway.BMC pulmonary medicine · 2024Article
- Increased ER Stress and Unfolded Protein Response Activation in Epithelial and Inflammatory Cells in Hypersensitivity Pneumonitis.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2024Article
- Animal models of acute exacerbation of pulmonary fibrosis.Respiratory research · 2023Review
- Regulation of epithelial transitional states in murine and human pulmonary fibrosis.The Journal of clinical investigation · 2023Article
- Variability of serum CYFRA 21 - 1 and its susceptibility to clinical characteristics in individuals without cancer: a 4-year retrospective analysis.BMC pulmonary medicine · 2023Article
- A systematic review of the research progress of traditional Chinese medicine against pulmonary fibrosis: from a pharmacological perspective.Chinese medicine · 2023Review
- Disruption of proteostasis causes IRE1 mediated reprogramming of alveolar epithelial cells.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Stem cells, cell therapies, and bioengineering in lung biology and disease 2021.American journal of physiology. Lung cellular and molecular physiology · 2022Review
- Why Should Natural Principles Be Simple?Philosophia (Ramat-Gan, Israel) · 2022Article
- Sensitization of the UPR by loss of PPP1R15A promotes fibrosis and senescence in IPF.Scientific reports · 2021Article
- COVID-19 and pulmonary fibrosis: A potential role for lung epithelial cells and fibroblasts.Immunological reviews · 2021Review
- CBClinical and translational medicine · 2021Article
- Cellular Senescence in Lung Fibrosis.International journal of molecular sciences · 2021Review
15 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
The incidence of idiopathic pulmonary fibrosis (IPF) increases with age. The mechanisms that underlie the age-dependent risk for IPF are unknown. Based on studies that suggest an association of IPF and γherpesvirus infection, we infected young (2-3 mo) and old (≥18 mo) C57BL/6 mice with the murine γherpesvirus 68. Acute murine γherpesvirus 68 infection in aging mice resulted in severe pneumonitis and fibrosis compared with young animals. Progressive clinical deterioration and lung fibrosis in the late chronic phase of infection was observed exclusively in old mice with diminution of tidal volume. Infected aging mice showed higher expression of transforming growth factor-β during the acute phase of infection. In addition, aging, infected mice showed elevation of proinflammatory cytokines and the fibrocyte recruitment chemokine, CXCL12, in bronchoalveolar lavage. Analyses of lytic virus infection and virus reactivation indicate that old mice were able to control chronic infection and elicit antivirus immune responses. However, old, infected mice showed a significant increase in apoptotic responses determined by in situ terminal deoxynucleotidyl transferase dUTP nick end labeling assay, levels of caspase-3, and expression of the proapoptotitc molecule, Bcl-2 interacting mediator. Apoptosis of type II lung epithelial cells in aging lungs was accompanied by up-regulation of endoplasmic reticulum stress marker, binding immunoglobulin protein, and splicing of X-box-binding protein 1. These results indicate that the aging lung is more susceptible to injury and fibrosis associated with endoplasmic reticulum stress, apoptosis of type II lung epithelial cells, and activation of profibrotic pathways.
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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.