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Single-cell and Spatial Transcriptomic Profiling Reveal that LAPTM5-mediated Ferroptosis in Macrophages Induces
Erli Wu1, Xuan Yin2, Yitong Chen1
1Stomatology Hospital, School of Stomatology, Zhejiang Provincial Clinical Research Center for Oral Diseases, Key Laboratory of Oral Biomedical Research of Zhejiang Province, Engineering Research Center of Oral Biomaterials and Devices of Zhejiang Province, Zhejiang University School of Medicine, Hangzhou, 310000, China.
Inflammation
|July 7, 2026
Summary
Ferroptosis, a cell death form, drives periodontitis inflammation by affecting macrophages and fibroblasts. Targeting LAPTM5 in macrophages may restore periodontal immune balance.
Area of Science:
- Immunology
- Cell Biology
- Genetics
Background:
- Periodontitis involves chronic inflammation and tissue damage.
- Programmed cell death (PCD) pathways are crucial for immune balance.
- The specific PCD pathway driving periodontitis remains unclear.
Purpose of the Study:
- To systematically analyze PCD gene expression in periodontitis.
- To identify the key PCD pathway contributing to periodontal inflammation.
- To explore the role of ferroptosis and its regulators in periodontitis.
Main Methods:
- Integrated single-cell RNA sequencing datasets.
- Applied gene set scoring and cell-cell communication analyses.
- Utilized machine learning to identify hub genes and performed gene knockdown experiments.
Main Results:
- Ferroptosis was identified as a significant PCD pathway in periodontitis, primarily in macrophages.
- Ferroptotic macrophages influenced fibroblast behavior, promoting inflammation.
- LAPTM5 was identified as a key gene regulating macrophage ferroptosis and fibroblast response.
Conclusions:
- Ferroptosis is a key pathogenic mechanism in periodontitis.
- LAPTM5-mediated macrophage ferroptosis drives fibroblast dysfunction and chronic inflammation.
- Targeting LAPTM5 offers potential therapeutic strategies for periodontitis.