ArticleScientific reports2017
Krüpple-like-factor 4 Attenuates Lung Fibrosis via Inhibiting Epithelial-mesenchymal Transition.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 63 citations in OpenAlex.
- Decoding fibroblast activation: Transcriptional networks in hepatic stellate cells and across fibrotic organs (Review).International journal of molecular medicine · 2026Review
- Article
- Osteoprotegerin-Enabled Immune Evasion of Pathological Adipose Stromal Cells Drives Metabolic Dysfunction in Obesity.bioRxiv : the preprint server for biology · 2026Article
- Machine learning identifies lipid-associated genes and constructs diagnostic and prognostic models for idiopathic pulmonary fibrosis.Orphanet journal of rare diseases · 2025Article
- FTO-mediated m6A demethylation of KLF4 promotes the proliferation and collagen deposition of keloid fibroblasts.Toxicology research · 2025Article
- Optimized rAAV8 targeting acinar KLF4 ameliorates fibrosis in chronic pancreatitis via exosomes-enriched let-7s suppressing pancreatic stellate cells activation.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- CircZNF609 regulates pulmonary fibrosis via miR-145-5p/KLF4 axis and its translation function.Cellular & molecular biology letters · 2023Article
- Mechanism of KLF9 in airway inflammation in chronic obstructive pulmonary.Immunity, inflammation and disease · 2023Article
- Overexpression of KLF4 Suppresses Pulmonary Fibrosis through the HIF-1α/Endoplasmic Reticulum Stress Signaling Pathway.International journal of molecular sciences · 2023Article
- Inhibition of miR-25 Ameliorates Cardiac Dysfunction and Fibrosis by Restoring Krüppel-like Factor 4 Expression.International journal of molecular sciences · 2023Article
- Review
- Single-Cell RNA-Seq Identifies Dynamic Cardiac Transition Program from ADCs Induced by Leukemia Inhibitory Factor.Stem cells (Dayton, Ohio) · 2022Article
- [AZD9291 suppresses proliferation and migration of nasopharyngeal carcinoma cells by inhibiting the PI3K-AKT-mTOR pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Article
- KLF4 is a therapeutically tractable brake on fibroblast activation that promotes resolution of pulmonary fibrosis.JCI insight · 2022Article
- KLF4 regulates TERT expression in alveolar epithelial cells in pulmonary fibrosis.Cell death & disease · 2022Article
- Transcriptional analysis of lung fibroblasts identifies PIM1 signaling as a driver of aging-associated persistent fibrosis.JCI insight · 2022Article
- Epithelial-mesenchymal transition and its transcription factors.Bioscience reports · 2022Review
- KLF4 Alleviates Hypertrophic Scar Fibrosis by Directly Activating BMP4 Transcription.International journal of biological sciences · 2022Article
- Distinct roles of KLF4 in mesenchymal cell subtypes during lung fibrogenesis.Nature communications · 2021Article
- Effect of almonertinib on the proliferation, invasion, and migration in non-small cell lung cancer cells.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2021Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial-mesenchymal transition (EMT) plays an important role in the pathogenesis of idiopathic pulmonary fibrosis (IPF). Krüpple-like-factor 4 (KLF4), has been suggested to play an important role in the phenotype transition. However, its function in pulmonary fibrosis and EMT of human alveolar epithelial cells (AECs) remains unclear. This study aimed to examine the role of KLF4 in pulmonary fibrosis and EMT. Decreased expression of KLF4 was first observed in human IPF lung tissues and models of bleomycin-induced pulmonary fibrosis. Transgenic mice with overexpression of KLF4 were subjected to bleomycin-induced pulmonary fibrosis model and showed attenuated lung fibrosis and EMT compared to wild type group. Furthermore, the effects overexpression and knockdown of KLF4 on TGF-β1-induced EMT were examined in AECs. Adenovirus-mediated overexpression of KLF4 attenuated TGF-β1-induced EMT and activation of Smad2/3 and Dvl in AECs. Conversely, knockdown of KLF4 promoted the activation of pathways above mentioned and TGF-β1-induced EMT. Our results demonstrates that KLF4 plays an important role in bleomycin-induced lung fibrosis through suppressing TGFβ1-induced EMT. Thus, it may serve as a potential target for the treatment of pulmonary fibrosis.
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