ArticleCytoJournal2025
Zinc finger and broad-complex, tramtrack, and bric-a-brac domain containing 16 silencing attenuates bleomycin-induced pulmonary fibrosis in mice through inhibition of the phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin pathway.
Article in CytoJournal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Zinc and animal health: an in-depth exploration of its role in physiological functions and regulatory molecular mechanisms.Journal of animal science and biotechnology · 2025Review
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Idiopathic pulmonary fibrosis (PF) is a chronic and life-threatening lung disease. This study aimed to investigate the role of zinc finger and BTB domain containing 16 (Zbtb16), a transcription factor, in the progression of PF by analyzing its expression and regulatory effects in mouse and cell models. Material and Methods: The gene expression profiles in bleomycin-induced (BL-I) PF lung tissues of mice were analyzed using the gene expression omnibus database. The mouse model of BL-I PF and cell model of transforming growth factor-β1 (TGF-β1)-induced mice lung epithelial cell (LEC) fibrosis was constructed. Zbtb16 expression was evaluated by reverse transcription quantitative polymerase chain reaction, Western blot, or immunohistochemistry. Tissue sections were assessed by hematoxylin and eosin, Masson, and terminal deoxynucleotidyl transferase dUTP nick-end labeling staining. The levels of protein, inflammation factors, and albumin were measured through Western blot or enzyme-linked immunosorbent assay. Results: Bioinformatics analysis found that Zbtb16 was the highest differentially expressed marker in BL-I PF mice. Zbtb16 was highly expressed in the mice and cell model. Zbtb16 silencing could reduce lung tissues' collagen deposition, pulmonary edema, and pulmonary apoptotic cells; improve vascular permeability; and decrease fibrosis markers and inflammation factors expressed in model mice. Zbtb16 silencing could reduce fibrosis markers and inflammation factor levels in the cell model ( Conclusion: This study identified Zbtb16 as a key regulator of PF progression, mediating its effects through the PAmT-P. Zbtb16 silencing alleviated fibrosis and inflammation
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