Mitophagy Contributes to the Pathogenesis of Inflammatory Diseases

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...

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Bibliographic Details
Published in:Inflammation 2018-10, Vol.41 (5), p.1590-1600
Main Authors: Zhao, Yan, Huang, Shaohui, Liu, Jie, Wu, Ximing, Zhou, Shuai, Dai, Ke, Kou, Yurong
Format: Article
Language:English
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
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Summary: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.
ISSN:0360-3997
1573-2576
DOI:10.1007/s10753-018-0835-2