ArticleInternational journal of molecular sciences2023
Overexpression of KLF4 Suppresses Pulmonary Fibrosis through the HIF-1α/Endoplasmic Reticulum Stress Signaling Pathway.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Decoding fibroblast activation: Transcriptional networks in hepatic stellate cells and across fibrotic organs (Review).International journal of molecular medicine · 2026Review
- Regulatory roles and translational potential of the Kruppel-like factor family in liver disease.iLIVER · 2026Review
- ANGII Initiated HSF2 Trans-Activating HIF-1α Through Induction of ER Stress to Promote Cardiac Hypertrophy.Clinical and experimental pharmacology & physiology · 2026Article
- Machine learning identifies lipid-associated genes and constructs diagnostic and prognostic models for idiopathic pulmonary fibrosis.Orphanet journal of rare diseases · 2025Article
- Identification of potential mechanisms of Schisandrin B in the treatment of idiopathic pulmonary fibrosis by integrating network pharmacology and experimental validation.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Review
- Vascular endothelial growth factor A: friend or foe in the pathogenesis of HIV and SARS-CoV-2 infections?Frontiers in cellular and infection microbiology · 2024Review
- Highlighting fibroblast plasticity in lung fibrosis: the WI-38 cell line as a model for investigating the myofibroblast and lipofibroblast switch.Theranostics · 2024Article
- Network Pharmacology and Machine Learning Reveal Salidroside's Mechanisms in Idiopathic Pulmonary Fibrosis Treatment.Journal of inflammation research · 2024Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
The hypoxia-inducible factor-1α/endoplasmic reticulum stress signaling pathway (HIF-1α/ERS) has a crucial role in the pathogenetic mechanism of pulmonary fibrosis (PF). However, the upstream regulatory mediators of this pathway remain unclear. In the present study, by conducting bioinformatics analysis, we found that Krüppel-like factor 4 (KLF4) expression was decreased in the lung tissues of patients with idiopathic pulmonary fibrosis (IPF) as compared to that in patients with non-IPF. Furthermore, KLF4 expression was significantly reduced (
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Registered trials
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