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Chaperone-mediated autophagy dysfunction in imiquimod-induced psoriasiform dermatitis
Wei Zhao1, Kainan Liao1, Wei Song1
1Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences of Anhui Medical University, Hefei, China.
Autophagy Reports
|August 28, 2025
Summary
Defective chaperone-mediated autophagy (CMA) contributes to psoriasis by increasing toll-like receptor 7 (TLR7). Activating CMA reduces skin lesion severity and keratinocyte abnormalities in this chronic inflammatory skin disease.
Area of Science:
- Dermatology
- Cell Biology
- Immunology
Background:
- Psoriasis is a chronic inflammatory skin disease driven by keratinocyte hyperproliferation and abnormal differentiation.
- Autophagy, a cellular degradation process, is implicated in psoriasis pathogenesis, but the role of chaperone-mediated autophagy (CMA) remains unclear.
Purpose of the Study:
- To investigate the role of chaperone-mediated autophagy (CMA) in keratinocytes during psoriasis development.
- To explore CMA's potential as a therapeutic target for psoriasis.
Main Methods:
- Utilized an imiquimod (IMQ)-induced mouse model of psoriasiform lesions.
- Assessed CMA activity, keratinocyte proliferation, differentiation, and cytokine secretion.
- Investigated the degradation of toll-like receptor 7 (TLR7) by CMA.
Main Results:
- Defective CMA was observed in IMQ-induced psoriasiform lesions.
- CMA activation significantly reduced skin lesion severity, keratinocyte proliferation, and differentiation.
- CMA deficiency led to increased TLR7 levels and enhanced TLR7-NF-κB signaling.
Conclusions:
- Defective CMA is a key feature in IMQ-induced psoriasis.
- Activating CMA ameliorates psoriatic phenotypes by modulating TLR7 signaling in keratinocytes.
- CMA represents a promising therapeutic target for psoriasis treatment.
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