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Critical Roles and Molecular Mechanisms of Chaperone-Mediated Autophagy in Infections
1Hengyang Medical School, University of South China, Hengyang 421001, China.
International Journal of Molecular Sciences
|February 13, 2026
Summary
Chaperone-mediated autophagy (CMA) is crucial for host defense during infections by degrading damaged proteins. Targeting CMA offers therapeutic potential, but its cell-specific roles require further investigation for optimal anti-infective strategies.
Area of Science:
- Cellular Biology
- Immunology
- Molecular Mechanisms
Background:
- Chaperone-mediated autophagy (CMA) is a selective lysosomal degradation pathway.
- CMA utilizes heat shock cognate 70 kDa protein (HSC70) and lysosomal receptor LAMP-2A to recognize and degrade KFERQ-like motif substrates.
- CMA is vital for cellular homeostasis and host defense against various pathogens.
Purpose of the Study:
- To review recent advancements in understanding CMA's role in viral, bacterial, and fungal infections.
- To identify key regulatory pathways and therapeutic targets within CMA.
- To highlight challenges in translating CMA modulation into clinical anti-infective strategies.
Main Methods:
- Literature review of recent studies on CMA in infectious contexts.
- Analysis of CMA's molecular mechanisms, including substrate recognition and lysosomal translocation.
- Examination of therapeutic strategies targeting CMA components like LAMP-2A and HSC70.
Main Results:
- CMA limits pathogen replication and mitigates infection-induced cellular stress.
- Progress has been made in identifying CMA's regulatory nodes and signaling pathways during infections.
- CMA modulation, such as stabilizing LAMP-2A, shows therapeutic promise.
Conclusions:
- CMA plays a significant role in host defense and cellular homeostasis during infections.
- Targeting CMA presents a potential therapeutic avenue for infectious diseases.
- Further research is needed to understand the spatiotemporal and cell-type-specific regulation of CMA for effective clinical translation.
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