Abstract
Autophagy is a general protective mechanism for maintaining homeostasis in eukaryotic cells, regulating cellular metabolism, and promoting cell survival by degrading and recycling cellular components under stress conditions. The degradation pathway that is mediated by autophagy receptors is called selective autophagy, also named as xenophagy. Autophagy receptor NDP52 acts as a ‘bridge’ between autophagy and the ubiquitin-proteasome system, and it also plays an important role in the process of selective autophagy. Pathogenic microbial infections cause various diseases in both humans and animals, posing a great threat to public health. Increasing evidence has revealed that autophagy and autophagy receptors are involved in the life cycle of pathogenic microbial infections. The interaction between autophagy receptor and pathogenic microorganism not only affects the replication of these microorganisms in the host cell, but it also affects the host’s immune system. This review aims to discuss the effects of autophagy on pathogenic microbial infection and replication, and summarizes the mechanisms by which autophagy receptors interact with microorganisms. While considering the role of autophagy receptors in microbial infection, NDP52 might be a potential target for developing effective therapies to treat pathogenic microbial infections.
Highlights
Macroautophagy is an internal balancing mechanism for maintaining homeostasis in eukaryotic cells
These findings indicate a close correlation between autophagy receptor NDP52 and bacterial infection [41]
Selective autophagy protects the cytoplasm from invading bacteria, during which NDP52 plays a center role in the recognition and binding to bacteria [51]
Summary
Macroautophagy (hereafter referred to as autophagy) is an internal balancing mechanism for maintaining homeostasis in eukaryotic cells. NDP52 is a member of the nuclear dots (NDs) protein family [25], which contains a SKICH30 domain at the amino terminus [26], the central region is a coiled-coil domain, and the carboxy. Researchers performed a structure-based prediction of protein interactions and discovered that the proteins of Salmonella, Listeria and Shigella can modify the selective autophagy receptors SQSTM1 and NDP52. These findings indicate a close correlation between autophagy receptor NDP52 and bacterial infection [41]. We will focus on the relationship between autophagy and bacteria, such as Salmonella, Listeria, Shigella, and Streptococcus, and reveal the role of autophagy in bacterial infection and clearance, as well as the specific mechanism of NDP52 in bacterial infection (Table 1).
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