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已发表论文
中性粒细胞胞外诱捕网通过抑制 PLK1 和细胞周期停滞损害脓毒症中的肺内皮细胞增殖
Authors Zhu C, Qu M, Wu D, Shi Y, Zeng F, Miao C, Zhou D
Received 2 August 2025
Accepted for publication 16 December 2025
Published 27 December 2025 Volume 2025:18 Pages 18165—18180
DOI https://doi.org/10.2147/JIR.S556891
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Anh Ngo
Chenyu Zhu,1– 3,* Mengdi Qu,1– 3,* Dan Wu,1– 3 Yuxin Shi,1– 3 Fu Zeng,1– 3 Changhong Miao,1– 3 Di Zhou1– 3
1Department of Anesthesiology, Zhongshan Hospital, Fudan University, Shanghai, People’s Republic of China; 2Shanghai Key Laboratory of Perioperative Stress and Protection, Zhongshan Hospital, Fudan University, Shanghai, People’s Republic of China; 3Department of Anesthesiology, Shanghai Medical College, Fudan University, Shanghai, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Di Zhou, Department of Anesthesiology, Zhongshan Hospital, Fudan University, 180# Feng-Lin Road, Shanghai, 200032, People’s Republic of China, Email judy612542@163.com Changhong Miao, Department of Anesthesiology, Zhongshan Hospital, Fudan University, 180# Feng-Lin Road, Shanghai, 200032, People’s Republic of China, Email miaochanghong_zs@163.com
Purpose: Sepsis continues to pose a significant threat to global health, characterized by elevated mortality rates. Pulmonary complications frequently develop in septic patients, with endothelial dysfunction correlating with adverse clinical outcomes. While overproduction of neutrophil extracellular traps (NETs) is implicated in vascular damage, their specific influence on the regenerative potential of pulmonary endothelial cells requires further elucidation. Our investigation aims to address this critical knowledge gap.
Patients and Methods: Clinical samples from sepsis patients and healthy controls were analyzed to establish the correlation between NETs and pulmonary endothelial injury. An in vivo sepsis model was generated through cecal ligation and puncture (CLP) in mice, with sham surgery animals serving as reference group. Human umbilical vein endothelial cells (HUVECs) were employed for in vitro assessment of NETs-mediated cell cycle modulation.
Results: Elevated NETs formation was observed in septic patients, showing positive association with inflammatory damage. CLP-induced mice demonstrated substantially increased NETs levels, pronounced pulmonary vascular permeability, and notable endothelial cell depletion. DNase I-mediated NETs degradation alleviated pulmonary inflammation and promoted endothelial recovery. Both experimental models revealed that excessive NETs release during sepsis compromises endothelial proliferation via polo-like kinase 1 (PLK1) pathway inhibition and subsequent G2/M phase arrest.
Conclusion: This study establishes that NETs accumulation in septic pulmonary injury hinders endothelial regeneration and vascular repair through PLK1 signaling suppression and G2/M cell cycle blockade.
Keywords: sepsis, NETs, endothelial dysfunction, polo like kinase 1, cell cycle
1Department of Anesthesiology, Zhongshan Hospital, Fudan University, Shanghai, People’s Republic of China; 2Shanghai Key Laboratory of Perioperative Stress and Protection, Zhongshan Hospital, Fudan University, Shanghai, People’s Republic of China; 3Department of Anesthesiology, Shanghai Medical College, Fudan University, Shanghai, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Di Zhou, Department of Anesthesiology, Zhongshan Hospital, Fudan University, 180# Feng-Lin Road, Shanghai, 200032, People’s Republic of China, Email judy612542@163.com Changhong Miao, Department of Anesthesiology, Zhongshan Hospital, Fudan University, 180# Feng-Lin Road, Shanghai, 200032, People’s Republic of China, Email miaochanghong_zs@163.com
Purpose: Sepsis continues to pose a significant threat to global health, characterized by elevated mortality rates. Pulmonary complications frequently develop in septic patients, with endothelial dysfunction correlating with adverse clinical outcomes. While overproduction of neutrophil extracellular traps (NETs) is implicated in vascular damage, their specific influence on the regenerative potential of pulmonary endothelial cells requires further elucidation. Our investigation aims to address this critical knowledge gap.
Patients and Methods: Clinical samples from sepsis patients and healthy controls were analyzed to establish the correlation between NETs and pulmonary endothelial injury. An in vivo sepsis model was generated through cecal ligation and puncture (CLP) in mice, with sham surgery animals serving as reference group. Human umbilical vein endothelial cells (HUVECs) were employed for in vitro assessment of NETs-mediated cell cycle modulation.
Results: Elevated NETs formation was observed in septic patients, showing positive association with inflammatory damage. CLP-induced mice demonstrated substantially increased NETs levels, pronounced pulmonary vascular permeability, and notable endothelial cell depletion. DNase I-mediated NETs degradation alleviated pulmonary inflammation and promoted endothelial recovery. Both experimental models revealed that excessive NETs release during sepsis compromises endothelial proliferation via polo-like kinase 1 (PLK1) pathway inhibition and subsequent G2/M phase arrest.
Conclusion: This study establishes that NETs accumulation in septic pulmonary injury hinders endothelial regeneration and vascular repair through PLK1 signaling suppression and G2/M cell cycle blockade.
Keywords: sepsis, NETs, endothelial dysfunction, polo like kinase 1, cell cycle