Abstract

Chaperone-mediated autophagy (CMA) is a selective mechanism for degradation of soluble cytosolic proteins is responsible for the timed degradation of 30% of cytosolic proteins under conditions of prolonged nutrient deprivation and stress. Molecular chaperones in the lysosomal lumen and in the cytosol and induce this proteolytic pathway. A central molecule for CMA is a receptor in the lysosomal membrane is known as the lysosome-associated membrane protein (LAMP) type 2A. The decrease in CMA leads to cells to be more prone to oxidative stresses and pathogenes. Furthermore, the decreased CMA in aging is stem from reduced LAMP-2A in the lysosomal membrane. Here, we describe the evidence in support of the contribution of chaperokines and CMA in viral infections.

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