| Literature DB >> 29959626 |
Yan Zhao1, Shaohui Huang2, Jie Liu3, Ximing Wu4, Shuai Zhou1, Ke Dai4, Yurong Kou5,6.
Abstract
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.Entities:
Keywords: PINK1; Parkin; inflammation; inflammatory diseases; mitophagy
Mesh:
Substances:
Year: 2018 PMID: 29959626 DOI: 10.1007/s10753-018-0835-2
Source DB: PubMed Journal: Inflammation ISSN: 0360-3997 Impact factor: 4.092