The Single-Cell Triaptosis Regulatory Pattern in the Immune Microenvironment of Keloids

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.

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.

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.

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.