The Role of Autophagy and Autophagy Receptor NDP52 in Microbial Infections

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 s...

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Veröffentlicht in:International journal of molecular sciences 2020-03, Vol.21 (6), p.2008
Hauptverfasser: Fan, Shuangqi, Wu, Keke, Zhao, Mengpo, Zhu, Erpeng, Ma, Shengming, Chen, Yuming, Ding, Hongxing, Yi, Lin, Zhao, Mingqiu, Chen, Jinding
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Sprache:eng
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Zusammenfassung: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.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms21062008