线粒体自噬调节NLRP3炎症小体活性改善动物健康的作用机制

doi:10.11843/j.issn.0366-6964.2024.04.010

Abstract

Abstract: Mitochondria will produce few amount of reactive oxygen species (ROS) in the process of oxidative phosphorylation. While mitochondria are stressed, mitochondrial depolarization and ROS production increase, causing either mitochondrial damage or an increase in the expression level of mitochondrial reactive oxygen species (mtROS). ROS, as an important medium for activating NLRP3, promotes the assembly and activation of NLRP3 inflammasomes, and triggers a variety of diseases in animal bodies, such as mastitis, endometritis, neurodegenerative diseases, etc. Mitochondrial autophagy, as a selective autophagy process, regulates the activity of NLRP3 inflammasomes by clearing damaged and excess mitochondria, and maintains normal physiological functions of cells. This article reviews the effects and mechanisms of mitochondrial autophagy regulating NLRP3 inflammasomes on animal health, in order to gain a deeper understanding of the impact of mitochondrial autophagy on NLRP3 inflammasome-related diseases and provide new prevention and treatment targets for animal health.

Key words: autophagy, mitochondria, inflammation, animals, body health

CLC Number:

LI Feifei, ZHANG Chenmiao, TONG Jinjin, JIANG Linshu. Research Progress on the Mechanism of Mitochondrial Autophagy Regulating the Activity of NLRP3 Inflammatory Corpuscles to Improve Animal Health[J]. Acta Veterinaria et Zootechnica Sinica, 2024, 55(4): 1446-1455.

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Research Progress on the Mechanism of Mitochondrial Autophagy Regulating the Activity of NLRP3 Inflammatory Corpuscles to Improve Animal Health

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