已发表论文

瘢痕疙瘩免疫微环境中单细胞三联体凋亡调控模式

 

Authors Xie J, Zhao S , Wu D, Feng Y, Ma C, Yan W, Wang M

Received 25 April 2025

Accepted for publication 8 September 2025

Published 24 September 2025 Volume 2025:18 Pages 2423—2437

DOI https://doi.org/10.2147/CCID.S536776

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Anne-Claire Fougerousse

Jiaheng Xie,1,2,* Songyun Zhao,3,* Dan Wu,4,* Yeqi Feng,5 Chenfeng Ma,6 Wei Yan,7 Ming Wang1 

1Department of Plastic and Aesthetic Surgery, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, Jiangsu, 210029, People’s Republic of China; 2Department of Plastic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, People’s Republic of China; 3Department of Plastic Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, People’s Republic of China; 4Department of Dermatology, Huashan Hospital, Fudan University, Shanghai, 200040, People’s Republic of China; 5Department of Dermatology, The First Affiliated Hospital, Nanjing Medical University, Nanjing, People’s Republic of China; 6Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, Jiangsu, 210029, People’s Republic of China; 7Department of Burn and Plastic Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, People’s Republic of China

*These authors contributed equally to this work

Correspondence: Ming Wang, Email wangming@jsph.org.cn Wei Yan, Email yan_wei@njmu.edu.cn

Introduction: Keloids are a complex pathological condition of the skin characterized by abnormal proliferation of fibrous tissue and excessive accumulation of extracellular matrix, typically following inflammation after skin injury. Understanding the regulatory mechanisms of immune cells involved in keloid formation is essential for the development of effective treatments.
Methods: This study integrated publicly available single-cell RNA sequencing (scRNA-seq) data with our own keloid scRNA-seq samples to investigate the role of triaptosis in shaping the immune microenvironment of keloids. We analyzed the composition and functional status of fibroblast and immune cell subpopulations.
Results: Immune cells in keloids, especially CD8+ T cells and macrophages, showed significant heterogeneity under the influence of triaptosis regulatory patterns. These triaptosis-associated immune cell clusters exhibited distinct signaling interference compared to mesenchymal fibroblasts and contributed to keloid development. Furthermore, ELMO2 was identified as a key gene with a potential causal relationship to keloids using Summary-data-based Mendelian Randomization and validated through immunofluorescence staining.
Conclusion: Our findings reveal the complexity of cell–cell interactions in the keloid immune microenvironment and highlight triaptosis as a potential regulatory mechanism in keloid pathogenesis. The identification of ELMO2 as a key factor offers a promising therapeutic target. This study lays a foundation for developing novel therapeutic strategies and encourages future investigations into the clinical application of triaptosis-related interventions for keloid treatment.

Keywords: keloids, single-cell RNA sequencing, immune microenvironment, triaptosis, ELMO2