ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
FGF2 Mediated USP42-PPARγ Axis Activation Ameliorates Liver Oxidative Damage and Promotes Regeneration.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Growth factor applications and clinical translation: advances and challenges.Annals of medicine · 2026Review
- Targeting the immune-metabolic axis reverses orthodontics-induced systemic pathology.Signal transduction and targeted therapy · 2026Article
- FXR overexpression promotes liver regeneration through inducing FGF2 activation in APAP-induced acute liver injury.Hepatology international · 2026Article
- FGF family in health and disease.Molecular biomedicine · 2026Review
- Mechanically Active Hydrogel for Healing Intestinal Fistulas through the YAP-Mediated Mechanosensitization of Intestinal Epithelial Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- FGF2 Mediated USP42-PPARγ Axis Activation Ameliorates Liver Oxidative Damage and Promotes Regeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
Liver regeneration is critical for maintaining whole-body homeostasis, especially under exposure to deadly chemical toxins. Understanding the molecular mechanisms underlying liver repair is critical for the development of intervention strategies to treat liver diseases. In this study, ubiquitin-specific Proteases 42 (USP42) is identified as a novel deubiquitinases (DUB) of peroxisome proliferators-activated receptor γ (PPARγ) in hepatocytes. This DUB interacted, deubiquitinated, and stabilized PPARγ, and increased PPARγ targeted proliferative and antioxidative gene expressions, which protects the liver from carbon tetrachloride (CCL4) induced oxidative injury and promotes liver regeneration. In addition, fibroblast growth factor 2 (FGF2) initiated USP42 expression and enhanced the interaction between USP42 and PPARγ during the liver regeneration process. Moreover, the PPARγ full agonist, rosiglitazone (RSG), possesses the ability to further reinforce the USP42-PPARγ interplay, which enlightens to construct of an extracellular vesicle-based targeting strategy to activate the liver USP42-PPARγ axis and promote liver regeneration. In summary, the work uncovers the importance of USP42-PPARγ axis-mediated liver tissue homeostasis and provides a promising regimen to target this protein-protein interplay for liver regeneration.
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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.