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已发表论文
脓毒症相关急性肺损伤中细胞死亡与 cGAS-STING 通路之间的相互作用
Authors Li X, Wang M, Li Y, Huang Y , Zhang X
Received 28 May 2025
Accepted for publication 9 September 2025
Published 26 September 2025 Volume 2025:18 Pages 13291—13312
DOI https://doi.org/10.2147/JIR.S543273
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Dr Anh Ngo
Xuelin Li,* Min Wang,* Yifan Li, Ying Huang, Xiangcheng Zhang
Department of Critical Care Medicine, The Affiliated Huaian No. 1 People’s Hospital of Nanjing Medical University, Huaian, Jiangsu, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Xiangcheng Zhang, Department of Critical Care Medicine, The Affiliated Huaian No. 1 People’s Hospital of Nanjing Medical University, Huaian, Jiangsu, People’s Republic of China, Email zhxc0318@163.com Ying Huang, Department of Critical Care Medicine, The Affiliated Huaian No. 1 People’s Hospital of Nanjing Medical University, Huaian, Jiangsu, People’s Republic of China, Email huangying5249@njmu.edu.cn
Abstract: Sepsis-associated acute lung injury (ALI) is a complex pathological condition characterized by dysregulated inflammatory responses and the activation of various cell death mechanisms. This review examines the interplay between cell death pathways and the cGAS-STING signaling pathway in sepsis-associated ALI. The cGAS-STING pathway, which recognizes pathogen-derived DNA to trigger innate immune responses, can exacerbate lung injury when dysregulated. Recent studies have revealed that apoptosis, pyroptosis, necroptosis, autophagy, ferroptosis, NETosis, and PANoptosis are all intricately linked to the cGAS-STING pathway. These cell death mechanisms interact synergistically to amplify inflammation and tissue damage. Targeting the cGAS-STING pathway has been shown to reduce both inflammation and cell death in sepsis-associated ALI. For instance, inhibiting the stimulator of interferon genes (STING) pathway can mitigate ferroptosis and inflammation in macrophages, suggesting its potential as a therapeutic target. Furthermore, exosome-based therapies that modulate immune responses and promote tissue repair are emerging as promising strategies for treating ALI. However, further research is needed to fully elucidate the specific mechanisms through which the cGAS-STING pathway regulates cell death and inflammation in ALI. Additionally, exploring combination therapies that integrate STING inhibitors with other treatments, such as anti-inflammatory agents, may offer improved clinical outcomes in sepsis-associated ALI.
Keywords: sepsis, ALI, cell death, cGAS-STING pathway, inflammatory response, therapeutic targets
Department of Critical Care Medicine, The Affiliated Huaian No. 1 People’s Hospital of Nanjing Medical University, Huaian, Jiangsu, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Xiangcheng Zhang, Department of Critical Care Medicine, The Affiliated Huaian No. 1 People’s Hospital of Nanjing Medical University, Huaian, Jiangsu, People’s Republic of China, Email zhxc0318@163.com Ying Huang, Department of Critical Care Medicine, The Affiliated Huaian No. 1 People’s Hospital of Nanjing Medical University, Huaian, Jiangsu, People’s Republic of China, Email huangying5249@njmu.edu.cn
Abstract: Sepsis-associated acute lung injury (ALI) is a complex pathological condition characterized by dysregulated inflammatory responses and the activation of various cell death mechanisms. This review examines the interplay between cell death pathways and the cGAS-STING signaling pathway in sepsis-associated ALI. The cGAS-STING pathway, which recognizes pathogen-derived DNA to trigger innate immune responses, can exacerbate lung injury when dysregulated. Recent studies have revealed that apoptosis, pyroptosis, necroptosis, autophagy, ferroptosis, NETosis, and PANoptosis are all intricately linked to the cGAS-STING pathway. These cell death mechanisms interact synergistically to amplify inflammation and tissue damage. Targeting the cGAS-STING pathway has been shown to reduce both inflammation and cell death in sepsis-associated ALI. For instance, inhibiting the stimulator of interferon genes (STING) pathway can mitigate ferroptosis and inflammation in macrophages, suggesting its potential as a therapeutic target. Furthermore, exosome-based therapies that modulate immune responses and promote tissue repair are emerging as promising strategies for treating ALI. However, further research is needed to fully elucidate the specific mechanisms through which the cGAS-STING pathway regulates cell death and inflammation in ALI. Additionally, exploring combination therapies that integrate STING inhibitors with other treatments, such as anti-inflammatory agents, may offer improved clinical outcomes in sepsis-associated ALI.
Keywords: sepsis, ALI, cell death, cGAS-STING pathway, inflammatory response, therapeutic targets