自噬
发病机制
粒体自噬
线粒体
炎症
细胞生物学
活性氧
生物
免疫学
生物化学
细胞凋亡
作者
Yan Zhao,Shaohui Huang,Jie Liu,Ximing Wu,Shuai Zhou,Ke Dai,Yurong Kou
出处
期刊:Inflammation
[Springer Science+Business Media]
日期:2018-06-29
卷期号:41 (5): 1590-1600
被引量:73
标识
DOI:10.1007/s10753-018-0835-2
摘要
Mitophagy is a metabolic process to remove excessive or damaged mitochondria in eukaryotic cells. It is well-known that mitochondria are one of the major sources of reactive oxygen species (ROS). Mitochondrial ROS and damage-associated molecular patterns (DAMPs) can activate inflammasomes to induce inflammatory responses. Once the activation is regulated improperly, excessive inflammation will bring about various tissue injuries, resulting in a series of diseases. However, the selective mitochondrial autophagy can specifically eliminate dysfunctional mitochondria to maintain mitochondrial homeostasis and protect against the hyperinflammation induced by ROS and DAMPs. Recent studies demonstrated that a variety of internal and external factors regulate several inflammatory diseases via altering the level of mitophagy. In this review, we summarize the latest research progress of mitophagy and focus on the inflammatory responses regulated by mitophagy, aiming to illuminate the role of mitophagy in inflammation and provide clues to the diagnosis and therapy of inflammatory diseases.
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