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已发表论文
炎症消退期间组蛋白乙酰化的调节
Authors Gong L, Lei J, Zhou Y, Zhang J, Wu L, Chen Y, Liu X, Li Y
Received 28 April 2025
Accepted for publication 11 October 2025
Published 22 October 2025 Volume 2025:14 Pages 1145—1158
DOI https://doi.org/10.2147/ITT.S537242
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Professor Michael Shurin
Li Gong,1,* Juan Lei,2,* Yu Zhou,2 Jiangang Zhang,2 Lei Wu,2 Yu Chen,2 Xudong Liu,2 Yongsheng Li1,2
1Department of Phase I Clinical Trial Ward, Chongqing Key Laboratory of Translational Research for Cancer Metastasis and Individualized Treatment, Chongqing University Cancer Hospital, Chongqing, People’s Republic of China; 2Department of Medical Oncology, Chongqing Key Laboratory of Translational Research for Cancer Metastasis and Individualized Treatment, Chongqing University Cancer Hospital, Chongqing, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Yongsheng Li, Email lys@cqu.edu.cn
Background: Inflammatory resolution is an active and coordinated process. Histone acetylation represents the primary epigenetic alteration associated with inflammatory diseases. However, the precise role of histone acetylation in the resolution of inflammation remains poorly understood.
Methods: Lipopolysaccharide (1 μg/mL, 10 ng/mL) and Escherichia coli (105 c.f.u. 106 c.f.u.) were employed to establish inflammatory models both in vitro and in vivo. UPLC-MS/MS was utilized to quantify acetyl CoA and lipid mediators. qPCR was conducted to assess the expression of specific genes. Flow cytometry analysis was performed to enumerate polymorphonuclear neutrophils and monocytes/macrophages. Histone acetylation was evaluated using Western blotting.
Results: Our analysis reveals that histone acetylation and acetyl CoA are temporally regulated during the inflammatory response. A low-dose challenge results in heightened histone acetylation and reduced acetyl CoA. Metabolic repatterning during the inflammatory response promotes the generation of acetyl CoA and histone acetylation. Furthermore, the overexpression of histone acetylation enhances the production of anti-inflammatory lipid mediators, particularly the specialized pro-resolving lipid mediators (SPMs).
Conclusion: These findings illustrate that histone acetylation is not only temporally and differentially regulated during inflammatory responses but also interacts with metabolic reprogramming to promote the production of SPMs, thereby facilitating inflammation resolution.
Keywords: histone acetylation, inflammation resolution, lipid mediators, SPMs
1Department of Phase I Clinical Trial Ward, Chongqing Key Laboratory of Translational Research for Cancer Metastasis and Individualized Treatment, Chongqing University Cancer Hospital, Chongqing, People’s Republic of China; 2Department of Medical Oncology, Chongqing Key Laboratory of Translational Research for Cancer Metastasis and Individualized Treatment, Chongqing University Cancer Hospital, Chongqing, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Yongsheng Li, Email lys@cqu.edu.cn
Background: Inflammatory resolution is an active and coordinated process. Histone acetylation represents the primary epigenetic alteration associated with inflammatory diseases. However, the precise role of histone acetylation in the resolution of inflammation remains poorly understood.
Methods: Lipopolysaccharide (1 μg/mL, 10 ng/mL) and Escherichia coli (105 c.f.u. 106 c.f.u.) were employed to establish inflammatory models both in vitro and in vivo. UPLC-MS/MS was utilized to quantify acetyl CoA and lipid mediators. qPCR was conducted to assess the expression of specific genes. Flow cytometry analysis was performed to enumerate polymorphonuclear neutrophils and monocytes/macrophages. Histone acetylation was evaluated using Western blotting.
Results: Our analysis reveals that histone acetylation and acetyl CoA are temporally regulated during the inflammatory response. A low-dose challenge results in heightened histone acetylation and reduced acetyl CoA. Metabolic repatterning during the inflammatory response promotes the generation of acetyl CoA and histone acetylation. Furthermore, the overexpression of histone acetylation enhances the production of anti-inflammatory lipid mediators, particularly the specialized pro-resolving lipid mediators (SPMs).
Conclusion: These findings illustrate that histone acetylation is not only temporally and differentially regulated during inflammatory responses but also interacts with metabolic reprogramming to promote the production of SPMs, thereby facilitating inflammation resolution.
Keywords: histone acetylation, inflammation resolution, lipid mediators, SPMs