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<p>This study explores the role of Sulfatase 1 (SULF1) in the progression of Chronic Obstructive Pulmonary Disease (COPD). SULF1, a modifying enzyme involved in various biological processes, was quantified in human serum using ELISA, and its correlation with lung function was analyzed. The in vivo function of SULF1 was investigated through CRISPR-mediated gene knockout (KO) in mice, and SULF1 overexpression was induced via adeno-associated virus (AAV). A COPD model was established by exposing mice to cigarette smoke (CS). Our findings revealed that SULF1 levels were elevated in the serum of COPD patients, where they negatively correlated with the FEV<sub>1</sub>/FVC ratio and the FEV<sub>1</sub>/FVC ratio annual decline. In CS-exposed mice, SULF1 expression was downregulated in lung tissues but increased in serum and bronchoalveolar lavage fluid (BALF). SULF1 KO mice exhibited more pronounced emphysematous changes following CS exposure, whereas SULF1 overexpression partially mitigated these lung alterations. Additionally, SULF1 was found to play a protective role in COPD progression through stable binding with Keratin 15 (KRT15). In conclusion, this study elucidates the role of SULF1 in COPD progression, providing novel insights into its pathogenesis and identifying potential therapeutic targets.</p>

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A novel protective role for SULF1 in chronic obstructive pulmonary disease through systemic compensation and binding to KRT15

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月22日

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  • Yu Liu,
  • Erkang Yi,
  • Yue Xi,
  • Yujie Zuo,
  • Hairong Wang,
  • Xiaoyu Wang,
  • Qianmei Wen,
  • Jingwei Zhang,
  • Xinyue Mei,
  • Haiqing Li,
  • Fan Wu,
  • Zihui Wang,
  • Qi Wan,
  • Gaoying Tang,
  • Xiaoyang Zheng,
  • Ruiting Sun,
  • Pixin Ran,
  • Yumin Zhou

摘要

This study explores the role of Sulfatase 1 (SULF1) in the progression of Chronic Obstructive Pulmonary Disease (COPD). SULF1, a modifying enzyme involved in various biological processes, was quantified in human serum using ELISA, and its correlation with lung function was analyzed. The in vivo function of SULF1 was investigated through CRISPR-mediated gene knockout (KO) in mice, and SULF1 overexpression was induced via adeno-associated virus (AAV). A COPD model was established by exposing mice to cigarette smoke (CS). Our findings revealed that SULF1 levels were elevated in the serum of COPD patients, where they negatively correlated with the FEV1/FVC ratio and the FEV1/FVC ratio annual decline. In CS-exposed mice, SULF1 expression was downregulated in lung tissues but increased in serum and bronchoalveolar lavage fluid (BALF). SULF1 KO mice exhibited more pronounced emphysematous changes following CS exposure, whereas SULF1 overexpression partially mitigated these lung alterations. Additionally, SULF1 was found to play a protective role in COPD progression through stable binding with Keratin 15 (KRT15). In conclusion, this study elucidates the role of SULF1 in COPD progression, providing novel insights into its pathogenesis and identifying potential therapeutic targets.