ArticleBMC pulmonary medicine2021
Tauroursodeoxycholic acid alleviates pulmonary endoplasmic reticulum stress and epithelial-mesenchymal transition in bleomycin-induced lung fibrosis.
Article in BMC pulmonary medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Inhaled Angiopoietin-Like 4 Antisense Oligonucleotide Therapy for Lung Injury and Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Genetic Determinants of Progressive Pulmonary Fibrosis: A Comprehensive Review.International journal of molecular sciences · 2025Review
- Plasma 4-hydroxynonenal estimates severity and prognosis in patients with acute exacerbation of chronic obstructive pulmonary disease.Scientific reports · 2025Article
- Shensiqigui tablets alleviate bleomycin-induced pulmonary fibrosis by inhibiting the hedgehog/wnt-β-catenin pathway.Histology and histopathology · 2025Article
- A Cross-Tissue Transcriptome-Wide Association Study Identified Susceptibility Genes for Intervertebral Disc Degeneration.JOR spine · 2025Article
- The gut-lung axis in severe pneumonia-related lung injury: mechanisms and therapeutic strategies.Frontiers in immunology · 2025Review
- Gui-zhi-fu-ling-wan alleviates bleomycin-induced pulmonary fibrosis through inhibiting epithelial-mesenchymal transition and ferroptosis.Frontiers in pharmacology · 2025Article
- Review
- The interactions of subcellular organelles in pulmonary fibrosis induced by carbon black nanoparticles: a comprehensive review.Archives of toxicology · 2024Review
- Dissecting causal relationships between immune cells, plasma metabolites, and COPD: a mediating Mendelian randomization study.Frontiers in immunology · 2024Article
- Effects of Natural Products through Inhibiting Endoplasmic Reticulum Stress on Attenuation of Idiopathic Pulmonary Fibrosis.Drug design, development and therapy · 2024Review
- Endoplasmic Reticulum Stress and the Lysosomal Pathway Play Crucial Roles in the Progression of βB2-Crystallin Mutation-Induced Congenital Cataracts in Mice.Investigative ophthalmology & visual science · 2023Article
- Endoplasmic reticulum homeostasis: a potential target for diabetic nephropathy.Frontiers in endocrinology · 2023Review
- Cigarette smoke restricts the ability of mesenchymal cells to support lung epithelial organoid formation.Frontiers in cell and developmental biology · 2023Article
- The Role of DNA Damage and Repair in Idiopathic Pulmonary Fibrosis.Antioxidants (Basel, Switzerland) · 2022Review
- A Single-Cell Network-Based Drug Repositioning Strategy for Post-COVID-19 Pulmonary Fibrosis.Pharmaceutics · 2022Article
- ROS and Endoplasmic Reticulum Stress in Pulmonary Disease.Frontiers in pharmacology · 2022Review
- Endoplasmic reticulum stress contributes to high-dose radiation-induced chronic mechanical and thermal neuropathic pain.Molecular painArticle
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
backgroundSeveral studies demonstrate that endoplasmic reticulum (ER) stress-mediated epithelial-mesenchymal transition (EMT) is involved in the process of bleomycin (BLM)-induced pulmonary fibrosis. Tauroursodeoxycholic acid (TUDCA), a bile acid with chaperone properties, is an inhibitor of ER stress. This study aimed to investigate the preventive effects of TUDCA on BLM-induced EMT and lung fibrosis.
methodsThe model of lung fibrosis was established by intratracheal injection with a single dose of BLM (3.0 mg/kg). In TUDCA + BLM group, mice were intraperitoneally injected with TUDCA (250 mg/kg) daily.
resultsBLM-induced alveolar septal destruction and inflammatory cell infiltration were alleviated by TUDCA. BLM-induced interstitial collagen deposition, as determined by Sirius Red staining, was attenuated by TUDCA. BLM-induced elevation of pulmonary α-smooth muscle actin (α-SMA) and reduction of pulmonary E-cadherin were attenuated by TUDCA. BLM-induced pulmonary Smad2/3 phosphorylation was suppressed by TUDCA. BLM-induced elevation of Ki67 and PCNA was inhibited by TUDCA in mice lungs. In addition, BLM-induced elevation of HO-1 (heme oxygenase-1) and 3-NT (3-nitrotyrosine) was alleviated by TUDCA. Finally, BLM-induced upregulation of pulmonary GRP78 and CHOP was attenuated by TUDCA.
conclusionsThese results provide evidence that TUDCA pretreatment inhibits Smad2/3-medited EMT and subsequent lung fibrosis partially through suppressing BLM-induced ER stress and oxidative stress.
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