Mitophagy Contributes to the Pathogenesis of Inflammatory Diseases

• Published in: Inflammation Vol. 41; no. 5; pp. 1590 - 1600
• Main Authors: Zhao, Yan, Huang, Shaohui, Liu, Jie, Wu, Ximing, Zhou, Shuai, Dai, Ke, Kou, Yurong
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.10.2018; Springer Nature B.V
• Subjects: Autophagy; Biomedical and Life Sciences; Biomedicine; Homeostasis; Humans; Immunology; Inflammasomes; Inflammasomes - metabolism; Inflammation - complications; Inflammation - etiology; Inflammatory diseases; Internal Medicine; Mitochondria; Mitochondrial Degradation; Mitophagy; Pathology; Phagocytosis; Pharmacology/Toxicology; Reactive oxygen species; Reactive Oxygen Species - metabolism; Review; Rheumatology; inflammatory diseases; mitophagy; PINK1; inflammation; Parkin
• ISSN: 0360-3997; 1573-2576
• DOI: 10.1007/s10753-018-0835-2

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.