ArticleInternational journal of molecular sciences2020
Transcriptomic Evaluation of Pulmonary Fibrosis-Related Genes: Utilization of Transgenic Mice with Modifying p38 Signal in the Lungs.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 23 citations in OpenAlex.
- Article
- Adiponectin suppresses stiffness-dependent, profibrotic activation of lung fibroblasts.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Macrophages as determinants and regulators of systemic sclerosis-related interstitial lung disease.Journal of translational medicine · 2024Article
- Geroprotective interventions converge on gene expression programs of reduced inflammation and restored fatty acid metabolism.GeroScience · 2024Article
- Triiodothyronine acts on DAO to regulate pulmonary fibrosis progression by facilitating cell senescence through the p53/p21 signaling pathway.Frontiers in pharmacology · 2024Article
- Treatment of Idiopathic Pulmonary Fibrosis by Inhaled Silybin Dry Powder Prepared via the Nanosuspension Spray Drying Technology.ACS pharmacology & translational science · 2023Article
- Arctiin-encapsulated DSPE-PEG bubble-like nanoparticles inhibit alveolar epithelial type 2 cell senescence to alleviate pulmonary fibrosisFrontiers in pharmacology · 2023Article
- Bioinformatic analysis of differentially expressed genes and pathways in idiopathic pulmonary fibrosis.Annals of translational medicine · 2021Article
- Pathophysiological Roles of Stress-Activated Protein Kinases in Pulmonary Fibrosis.International journal of molecular sciences · 2021Review
- p38 Signalling Pathway.International journal of molecular sciences · 2021Article
- Identification and Validation of Potential Biomarkers and Pathways for Idiopathic Pulmonary Fibrosis by Comprehensive Bioinformatics Analysis.BioMed research international · 2021Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a progressive fibrosing lung disease that is caused by the dysregulation of alveolar epithelial type II cells (AEC II). The mechanisms involved in the progression of IPF remain incompletely understood, although the immune response accompanied by p38 mitogen-activated protein kinase (MAPK) activation may contribute to some of them. This study aimed to examine the association of p38 activity in the lungs with bleomycin (BLM)-induced pulmonary fibrosis and its transcriptomic profiling. Accordingly, we evaluated BLM-induced pulmonary fibrosis during an active fibrosis phase in three genotypes of mice carrying stepwise variations in intrinsic p38 activity in the AEC II and performed RNA sequencing of their lungs. Stepwise elevation of p38 signaling in the lungs of the three genotypes was correlated with increased severity of BLM-induced pulmonary fibrosis exhibiting reduced static compliance and higher collagen content. Transcriptome analysis of these lung samples also showed that the enhanced p38 signaling in the lungs was associated with increased transcription of the genes driving the p38 MAPK pathway and differentially expressed genes elicited by BLM, including those related to fibrosis as well as the immune system. Our findings underscore the significance of p38 MAPK in the progression of pulmonary fibrosis.
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