Abstract

Current research investigating autophagy, a complex catabolic process, indicates a vital role for this phenomenon. It is known that during the “self-eating” process, cell isolates portions of the cytoplasm or whole organelles in structures called autophagolisosomes, which are degraded by lysosomal hydrolases into macromolecules as an energy source during different situations. Autophagy is also responsible for cellular “self-cleaning” by removal of malformed macromolecular aggregates. Several recent studies have shown that during stress such as malnutrition or lack of oxygen and neurodegenerative diseases and cancer, autophagy plays an important role. In this review, structural and molecular aspects of autophagy, current detection techniques and their involvement in pathological processes, with emphasis in infectious diseases, are discussed. Bacteria such as Streptococcus pyogenes, Salmonella enterica, Listeria monocytogenes and hepatitis C virus and herpes simplex virus induce autophagy in infected cells. Leishmania amazonensis a parasite of macrophages causes cutaneous leishmaniasis in humans, induce autophagy in infected cells and skin tissue of experimental model; autophagy inhibitor treatment reduces the macrophage parasite load. These results provide evidences that autophagy modulation is important in the course of various infectious diseases, and perspectives of autophagy modulators treatments against various diseases in humans.

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