ArticleGenes & diseases2024
LKB1 depletion-mediated epithelial-mesenchymal transition induces fibroblast activation in lung fibrosis.
Article in Genes & diseases, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Deficiency of GCN5 exacerbates pulmonary fibrosis by disrupting the LKB1-AMPK pathway.Cell communication and signaling : CCS · 2026Article
- miR-3662 targets CAB39L to promote proliferation and invasion in gastric cancer.Clinical and experimental medicine · 2025Article
- Role of Interleukin-6 in Rheumatoid Arthritis-Associated Interstitial Lung Disease: Focus on the JAK/STAT Pathway and Macrophage Polarization.Journal of inflammation research · 2025Review
- Interleukin-9 promotes EMT-mediated PMArchives of toxicology · 2024Article
- Dysregulated bidirectional epithelial-mesenchymal crosstalk: a core determinant of lung fibrosis progression.Chinese medical journal pulmonary and critical care medicine · 2024Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
The factors that determine fibrosis progression or normal tissue repair are largely unknown. We previously demonstrated that autophagy inhibition-mediated epithelial-mesenchymal transition (EMT) in human alveolar epithelial type II (ATII) cells augments local myofibroblast differentiation in pulmonary fibrosis by paracrine signalling. Here, we report that liver kinase B1 (LKB1) inactivation in ATII cells inhibits autophagy and induces EMT as a consequence. In IPF lungs, this is caused by downregulation of
Identifiers
What OpenQuestion holds
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.