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已发表论文
STK11 通过磷酸化 AMPK 激活自噬减轻急性肺损伤期间的肺部炎症（在 A549 细胞模型中）
Authors Xiao R, Qi Z, Chen T, Wei F
Received 9 July 2025
Accepted for publication 11 December 2025
Published 19 December 2025 Volume 2025:18 Pages 17789—17802
DOI https://doi.org/10.2147/JIR.S548864
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Cynthia Koziol-White
Rong Xiao,1 Zhimin Qi,1 Ting Chen,2 Fusheng Wei2
1Department of Anesthesiology and Operation, The Affiliated Stomatological Hospital, Jiangxi Medical College, Nanchang University, Jiangxi Provincial Key Laboratory of Oral Diseases, Jiangxi Provincial Clinical Research Center for Oral Diseases, Nanchang, 330000, People’s Republic of China; 2Department of Anesthesiology and Operation, the First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, 330000, People’s Republic of China
Correspondence: Fusheng Wei, Department of Anesthesiology and Operation, The First Affiliated Hospital of Jiangxi MedicaL College, Nanchang University, No. 1519, Dongyue Avenue, Xianghu New Town, Nanchang, 330000, People’s Republic of China, Email ndyfy02221@ncu.edu.cn
Purpose: To investigate if protein STK11 alleviates lipopolysaccharide-induced acute lung injury (ALI), hypothesizing it activates autophagy (harmful substance clearance) via AMPK’s “start signal”.
Methods: Researchers used a genomics-first approach: they integrated datasets GSE66890, GSE10474, and GSE32707, screened autophagy-related differentially expressed genes in ALI via bioinformatics, and confirmed STK11 as a key regulator through protein-protein interaction analysis. They treated human lung cells with 50 μg/mL lipopolysaccharide for 24 hours to establish ALI models, then overexpressed or silenced STK11 in the cells. They assessed cell function, apoptosis, inflammatory factors, autophagy activity, and AMPK activation.
Results: Researchers verified STK11 as a key regulator of autophagy in ALI. STK11 overexpression significantly improved cell function, reduced apoptosis (lower pro-apoptotic/higher anti-apoptotic proteins), decreased IL-6/IL-8/TNF-α (mRNA/protein levels), enhanced autophagy (elevated LC3B-II, reduced P62, more autophagosomes), and activated AMPK. STK11 silencing reversed these protective effects and inhibited AMPK.
Conclusion: STK11 mitigates lipopolysaccharide-induced lung cell damage by activating AMPK-mediated autophagy, emerging as a potential therapeutic target for ALI.
Keywords: STK11, AMPK, acute lung injury, inflammation, autophagy, LPS
1Department of Anesthesiology and Operation, The Affiliated Stomatological Hospital, Jiangxi Medical College, Nanchang University, Jiangxi Provincial Key Laboratory of Oral Diseases, Jiangxi Provincial Clinical Research Center for Oral Diseases, Nanchang, 330000, People’s Republic of China; 2Department of Anesthesiology and Operation, the First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, 330000, People’s Republic of China
Correspondence: Fusheng Wei, Department of Anesthesiology and Operation, The First Affiliated Hospital of Jiangxi MedicaL College, Nanchang University, No. 1519, Dongyue Avenue, Xianghu New Town, Nanchang, 330000, People’s Republic of China, Email ndyfy02221@ncu.edu.cn
Purpose: To investigate if protein STK11 alleviates lipopolysaccharide-induced acute lung injury (ALI), hypothesizing it activates autophagy (harmful substance clearance) via AMPK’s “start signal”.
Methods: Researchers used a genomics-first approach: they integrated datasets GSE66890, GSE10474, and GSE32707, screened autophagy-related differentially expressed genes in ALI via bioinformatics, and confirmed STK11 as a key regulator through protein-protein interaction analysis. They treated human lung cells with 50 μg/mL lipopolysaccharide for 24 hours to establish ALI models, then overexpressed or silenced STK11 in the cells. They assessed cell function, apoptosis, inflammatory factors, autophagy activity, and AMPK activation.
Results: Researchers verified STK11 as a key regulator of autophagy in ALI. STK11 overexpression significantly improved cell function, reduced apoptosis (lower pro-apoptotic/higher anti-apoptotic proteins), decreased IL-6/IL-8/TNF-α (mRNA/protein levels), enhanced autophagy (elevated LC3B-II, reduced P62, more autophagosomes), and activated AMPK. STK11 silencing reversed these protective effects and inhibited AMPK.
Conclusion: STK11 mitigates lipopolysaccharide-induced lung cell damage by activating AMPK-mediated autophagy, emerging as a potential therapeutic target for ALI.
Keywords: STK11, AMPK, acute lung injury, inflammation, autophagy, LPS