A novel protective role for SULF1 in chronic obstructive pulmonary disease through systemic compensation and binding to KRT15.
6 affiliations
- 1State Key Laboratory of Respiratory Diseases, National Clinical Research Center for Respiratory Diseases, Guangzhou Institute of Respiratory Health, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, 195 Dongfeng Xi Road, Guangzhou, Guangdong, 510182, China.
- 2Guangzhou National Laboratory, Guangzhou International BioIsland, No.9 Xing Dao Huan Bei Road, Guangzhou, Guangdong, 510005, China.
- 3State Key Laboratory of Respiratory Diseases, National Clinical Research Center for Respiratory Diseases, Guangzhou Institute of Respiratory Health, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, 195 Dongfeng Xi Road, Guangzhou, Guangdong, 510182, China. [email protected].
- 4Guangzhou National Laboratory, Guangzhou International BioIsland, No.9 Xing Dao Huan Bei Road, Guangzhou, Guangdong, 510005, China. [email protected].
- 5State Key Laboratory of Respiratory Diseases, National Clinical Research Center for Respiratory Diseases, Guangzhou Institute of Respiratory Health, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, 195 Dongfeng Xi Road, Guangzhou, Guangdong, 510182, China. [email protected].
- 6Guangzhou National Laboratory, Guangzhou International BioIsland, No.9 Xing Dao Huan Bei Road, Guangzhou, Guangdong, 510005, China. [email protected].
Abstract
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.
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BibTeX
@article{liu2026novel,
title = {{A novel protective role for SULF1 in chronic obstructive pulmonary disease through systemic compensation and binding to KRT15.}},
author = {Yu Liu and Erkang Yi and Yue Xi and Yujie Zuo and Hairong Wang and Xiaoyu Wang and Qianmei Wen and Jingwei Zhang and Xinyue Mei and Haiqing Li and Fan Wu and Zihui Wang and Qi Wan and Gaoying Tang and Xiaoyang Zheng and Ruiting Sun and Pixin Ran and Yumin Zhou},
journal = {Respiratory research},
year = {2026},
month = jul,
doi = {10.1186/s12931-026-03818-9},
url = {https://europepmc.org/article/MED/42894165},
note = {CC BY-NC-ND},
}
RIS
TY - JOUR
TI - A novel protective role for SULF1 in chronic obstructive pulmonary disease through systemic compensation and binding to KRT15.
AU - Yu Liu
AU - Erkang Yi
AU - Yue Xi
AU - Yujie Zuo
AU - Hairong Wang
AU - Xiaoyu Wang
AU - Qianmei Wen
AU - Jingwei Zhang
AU - Xinyue Mei
AU - Haiqing Li
AU - Fan Wu
AU - Zihui Wang
AU - Qi Wan
AU - Gaoying Tang
AU - Xiaoyang Zheng
AU - Ruiting Sun
AU - Pixin Ran
AU - Yumin Zhou
PY - 2026
DA - 2026/07/01
JO - Respiratory research
DO - 10.1186/s12931-026-03818-9
UR - https://europepmc.org/article/MED/42894165
AB - 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.
SN - 1465-9921
SN - 1465-993X
ER -