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Updated: May 12, 2026
09:10
siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells
Published on: October 28, 2019
Integrative Transcriptomic and Single-Cell Analysis Reveals the Role of Autophagy-Related Genes in Psoriasis
Ying Zhou1,2, Bingjie Chen1,2, Junming Chen1,2
1Institute of Dermatology and Venereal Diseases, Department of Dermatology and Venereal Diseases, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, People's Republic of China.
Clinical, Cosmetic and Investigational Dermatology
|May 11, 2026
Summary
This study reveals that autophagy deficiency in psoriasis keratinocytes, driven by mTORC1 hyperactivation, impairs immune surveillance. Key genes PKP3, SPRR2B, and KRT6B are upregulated, offering potential therapeutic targets for psoriasis treatment.
Area of Science:
- Dermatology and Immunology
- Molecular Biology
- Systems Biology
Background:
- Psoriasis is a chronic inflammatory skin condition marked by abnormal keratinocyte behavior.
- Understanding the role of autophagy in psoriasis pathogenesis is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the regulatory mechanisms and key genes involved in autophagy during psoriasis.
- To identify potential therapeutic targets for modulating autophagy in psoriasis.
Main Methods:
- Single-cell RNA sequencing (scRNA-seq) data from psoriasis and normal samples were analyzed using pseudotime trajectory and cell communication analysis.
- Autophagy-related genes were intersected with differentially expressed genes, followed by protein-protein interaction (PPI) analysis to identify hub genes.
- Candidate hub gene expression was validated in clinical cohorts and mouse models.
Main Results:
- Autophagically active cells were enriched in psoriatic keratinocytes, with downregulated Renin angiotensin system (RAS) and NOD-like receptor signaling pathways.
- Enhanced HLA-E-CD94/NKG2A inhibitory signals and weakened KLRK1 activating signals were observed, linked to mTORC1 hyperactivation and autophagy deficiency.
- PKP3, SPRR2B, and KRT6B were identified as significantly upregulated hub genes in both mouse models and human psoriasis cohorts.
Conclusions:
- Autophagy-related genes, particularly PKP3, SPRR2B, and KRT6B, play a significant role in keratinocyte dysfunction and inflammation in psoriasis.
- The findings highlight potential therapeutic strategies targeting autophagy modulation for psoriasis treatment.
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