Toxicological Research

Korean Society of Toxicology & Korea Environmental Mutagen Society (한국독성학회)
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Enhancement of renal fibrosis in PHF20 transgenic mice

  • Uijin Juang (Department of Pharmacology, College of Medicine, Chungnam National University) ;
  • Soohyeon Lee (Department of Pharmacology, College of Medicine, Chungnam National University) ;
  • Suhwan Gwon (Department of Pharmacology, College of Medicine, Chungnam National University) ;
  • Woohyeong Jung (Department of Pharmacology, College of Medicine, Chungnam National University) ;
  • Huonggiang Nguyen (Department of Pharmacology, College of Medicine, Chungnam National University) ;
  • Qingzhi Huang (Department of Pharmacology, College of Medicine, Chungnam National University) ;
  • Beomwoo Lee (Department of Pharmacology, College of Medicine, Chungnam National University) ;
  • So Hee Kwon (College of Pharmacy, Yonsei Institute of Pharmaceutical Sciences, Yonsei University) ;
  • Seon-Hwan Kim (Department of Neurosurgery, Institute for Cancer Research, College of Medicine, Chungnam National University) ;
  • In Soo Kim (Department of Pharmacology, College of Medicine, Chungnam National University) ;
  • Jongsun Park (Department of Pharmacology, College of Medicine, Chungnam National University)
  • Received : 2024.07.21
  • Accepted : 2024.11.06
  • Published : 2025.01.15
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Abstract

Plant homeodomain finger protein 20 (PHF20) plays a crucial role in various biological processes, but its involvement in renal fibrosis remains unclear. This study investigated the role of PHF20 in renal fibrosis using a unilateral ureteral obstruction (UUO) mouse model, a widely accepted model for chronic kidney disease. PHF20 transgenic (PHF20-TG) and wildtype (WT) mice were utilized to explore how PHF20 influences renal inflammation and fibrosis. After UUO surgery, serum analysis revealed elevated creatinine levels and increased inflammatory markers, indicating worsened renal function in PHF20-TG mice. Histological analyses, including H&E, PAS, and Sirius Red staining, confirmed significant tissue damage and fibrosis in the PHF20-TG group. Molecular investigations demonstrated enhanced activation of the TGF-β/SMAD2/3 and NF-κB signaling pathways, both of which are crucial in the progression of renal fibrosis. Our findings suggest that PHF20 overexpression accelerates early-stage renal fibrosis by amplifying inflammatory responses and promoting collagen deposition. This indicates that PHF20 expression could serve as an early marker for renal fibrosis progression.

Keywords

Acknowledgement

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