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Polystyrene microplastics facilitate renal fibrosis through accelerating tubular epithelial cell senescence.
Pan, Chun; Wang, Xinglong; Fan, Zhencheng; Mao, Wenwen; Shi, Yujie; Wu, Yin; Liu, Tingting; Xu, Zhuobin; Wang, Huihui; Chen, Hao.
Afiliación
  • Pan C; Institute of Translational Medicine, Medical College, Yangzhou University, Yangzhou, China.
  • Wang X; Department of Orthopedics, The Fifth People's Hospital of Huai'an, Huai'an, China.
  • Fan Z; Institute of Translational Medicine, Medical College, Yangzhou University, Yangzhou, China.
  • Mao W; Institute of Translational Medicine, Medical College, Yangzhou University, Yangzhou, China.
  • Shi Y; Institute of Translational Medicine, Medical College, Yangzhou University, Yangzhou, China.
  • Wu Y; Department of Orthopedics, Affiliated Hospital of Yangzhou University, Yangzhou, China; Institute of Translational Medicine, Medical College, Yangzhou University, Yangzhou, China.
  • Liu T; Department of Orthopedics, Affiliated Hospital of Yangzhou University, Yangzhou, China.
  • Xu Z; Institute of Translational Medicine, Medical College, Yangzhou University, Yangzhou, China.
  • Wang H; Institute of Translational Medicine, Medical College, Yangzhou University, Yangzhou, China.
  • Chen H; Department of Orthopedics, Affiliated Hospital of Yangzhou University, Yangzhou, China. Electronic address: hchen2020@yzu.edu.cn.
Food Chem Toxicol ; 191: 114888, 2024 Sep.
Article en En | MEDLINE | ID: mdl-39053876
ABSTRACT
Microplastics (MPs), emerging contaminants, are easily transported and enriched in the kidney, suggesting the kidney is susceptible to the toxicity of MPs. In this study, we explored the toxicity of MPs, including unmodified polystyrene (PS), negative-charged PS-SO3H, and positive-charged PS-NH2 MPs, in mice models for 28 days at a human equivalent concentration. The results showed MPs significantly increased levels of UREA, urea nitrogen (BUN), creatinine (CREA), and uric acid (UA) levels in serum and white blood cells, protein, and microalbumin in urine. In the kidney, MPs triggered persistent inflammation and renal fibrosis, which was caused by the increased senescence of tubular epithelial cells. Moreover, we identified the critical role of the Klotho/Wnt/ß-catenin signaling pathway in the process of MPs induced senescence of tubular epithelial cells, promoting the epithelial-mesenchymal transformation of epithelial cells. MPs supported the secretion of TGF-ß1 by senescent epithelial cells and induced the activation of renal fibroblasts. On the contrary, restoring the function of Klotho can alleviate the senescence of epithelial cells and reverse the activation of fibroblasts. Thus, our study revealed new evidence between MPs and renal fibrosis, and adds an important piece to the whole picture of the plastic pollution on people's health.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Poliestirenos / Fibrosis / Senescencia Celular / Células Epiteliales / Microplásticos Límite: Animals / Humans / Male Idioma: En Revista: Food Chem Toxicol Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Reino Unido

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Poliestirenos / Fibrosis / Senescencia Celular / Células Epiteliales / Microplásticos Límite: Animals / Humans / Male Idioma: En Revista: Food Chem Toxicol Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Reino Unido