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已发表论文
eNAMPT-整合素α5β1轴介导中性粒细胞-内皮细胞相互作用驱动溃疡性结肠炎炎症
Authors Di Y, Ji W, Xiong W, Song W, Chen G, Li D, Qi F
Received 19 July 2025
Accepted for publication 8 November 2025
Published 30 December 2025 Volume 2025:18 Pages 18307—18321
DOI https://doi.org/10.2147/JIR.S554975
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Nadia Andrea Andreani
Yongcheng Di,1,2,* Wenbin Ji,1,2,* Wenhao Xiong,1,2,* Wenbin Song,1,2 Guoshan Chen,1,2 Danzhou Li,1,2 Feng Qi1,2
1Department of General Surgery, Tianjin Medical University General Hospital, Tianjin, People’s Republic of China; 2Tianjin Key Laboratory of Precise Vascular Reconstruction and Organ Function Repair, Tianjin, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Feng Qi, Email fengqi01@tmu.edu.cn
Background: Ulcerative colitis (UC), a chronic inflammatory bowel disease with rising global incidence, involves neutrophil-driven mucosal damage. The precise mechanisms remain elusive, hindering targeted therapies. Therefore, this study aims to integrate single-cell transcriptomics with in vivo experiments to reveal the key signaling axes driving pathogenic neutrophil activation in UC.
Methods: Single-cell transcriptomics characterized UC inflammatory microenvironments, focusing on neutrophil functional states and intercellular interactions. Based on key findings from bioinformatics analysis, we hypothesize that the eNAMPT-integrin α 5β 1 signaling axis drives abnormal neutrophil-endothelial cell communication and functionally validate this hypothesis in in vivo models.
Results: Neutrophils exhibited aberrant activation and significant NAMPT overexpression in UC. Extracellular eNAMPT functioned as a signaling molecule binding endothelial integrin α 5β 1, mediating pathological neutrophil-endothelial crosstalk. Pharmacological blockade of the eNAMPT/integrin α 5β 1 axis inhibited neutrophil mucosal infiltration, reducing inflammation and tissue damage in UC mouse models.
Conclusion: The eNAMPT-integrin α 5β 1-mediated neutrophil-endothelial communication axis represents a novel pathogenic pathway in UC, providing a foundation for precision therapies targeting this mechanism.
Keywords: ulcerative colitis, neutrophils, endothelial cells, NAMPT, bioinformatics
1Department of General Surgery, Tianjin Medical University General Hospital, Tianjin, People’s Republic of China; 2Tianjin Key Laboratory of Precise Vascular Reconstruction and Organ Function Repair, Tianjin, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Feng Qi, Email fengqi01@tmu.edu.cn
Background: Ulcerative colitis (UC), a chronic inflammatory bowel disease with rising global incidence, involves neutrophil-driven mucosal damage. The precise mechanisms remain elusive, hindering targeted therapies. Therefore, this study aims to integrate single-cell transcriptomics with in vivo experiments to reveal the key signaling axes driving pathogenic neutrophil activation in UC.
Methods: Single-cell transcriptomics characterized UC inflammatory microenvironments, focusing on neutrophil functional states and intercellular interactions. Based on key findings from bioinformatics analysis, we hypothesize that the eNAMPT-integrin α 5β 1 signaling axis drives abnormal neutrophil-endothelial cell communication and functionally validate this hypothesis in in vivo models.
Results: Neutrophils exhibited aberrant activation and significant NAMPT overexpression in UC. Extracellular eNAMPT functioned as a signaling molecule binding endothelial integrin α 5β 1, mediating pathological neutrophil-endothelial crosstalk. Pharmacological blockade of the eNAMPT/integrin α 5β 1 axis inhibited neutrophil mucosal infiltration, reducing inflammation and tissue damage in UC mouse models.
Conclusion: The eNAMPT-integrin α 5β 1-mediated neutrophil-endothelial communication axis represents a novel pathogenic pathway in UC, providing a foundation for precision therapies targeting this mechanism.
Keywords: ulcerative colitis, neutrophils, endothelial cells, NAMPT, bioinformatics