ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Nobiletin's role in idiopathic pulmonary fibrosis via the PI3K/AKT/MDM2/p53 signaling pathway.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Nobiletin as a Geroprotective Flavonoid: Mechanisms of Action, Therapeutic Potential, and Challenges of Bioavailability.Antioxidants (Basel, Switzerland) · 2026Review
- Krüppel-like factor 14 enhances fatty acid oxidation to combat pulmonary fibrosis.Respiratory research · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
To explore the therapeutic effects of Nobiletin (NOB) on Idiopathic pulmonary fibrosis (IPF) and to identify its targets and molecular pathways. We verified the inhibitory effect of NOB on the senescence of A549 cells through in vitro experiments, and the inhibitory effect of NOB on the migration ability of fibroblasts was verified by the Transwell experiment. The inhibitory effects of NOB on Idiopathic IPF were subsequently assessed in a mouse model induced by bleomycin (BLM). Through PPI network, gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, the PI3K/AKT/MDM2/p53 signaling pathway was identified as the critical pathway. The key proteins in the signaling pathway were verified by molecular docking and western blotting. NOB showed a great inhibitory effect on A549 cell senescence and Fibroblast migration. Meanwhile, NOB reduced BLM-induced collagen deposition in mouse lung tissues and inhibited alveolar epithelial cell (AEC) senescence. Through PPI network, P53 was screened as a core target of NOB. According to functional enrichment analysis results, the PI3K/AKT signaling was believed to have played an important role. Therefore, we speculate that the PI3K/AKT/MDM2/p53 signaling pathway mediated NOB's impact on IPF. These findings were validated through molecular docking and western blotting. This study demonstrated that NOB suppressed cell senescence to protect IPF through mediating the PI3K/AKT/MDM2/p53 signaling pathway.
Indexed as
Identifiers
40600992What 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.