Mitophagy Contributes to the Pathogenesis of Inflammatory Diseases
- PDF / 654,457 Bytes
- 11 Pages / 595.276 x 790.866 pts Page_size
- 6 Downloads / 204 Views
REVIEW
Mitophagy Contributes to the Pathogenesis of Inflammatory Diseases Yan Zhao,1 Shaohui Huang,2 Jie Liu,3 Ximing Wu,4 Shuai Zhou,1 Ke Dai,4 and Yurong Kou1,4,5
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. KEY WORDS: mitophagy; inflammation; inflammatory diseases; Parkin; PINK1.
MITOPHAGY Mitochondria, the main organelles for biological oxidation and energy conversion in all eukaryotic cells, provide energy for cell metabolism and other physiology activities, exerting a crucial function in cell homeostasis. Mitochondria synthesize respiratory chain protein complex by translating its own DNA and then produce ATP to meet the cellular energy requirements [1]. In the process of ATP 1
Department of Periodontology, School of Stomatology, China Medical University, Shenyang, 110002, China 2 Department of Oral and Maxillofacial Surgery, School of Stomatology, China Medical University, Shenyang, 110002, China 3 Science experiment Center, China Medical University, Shenyang, 110122, China 4 Department of Oral Biology, School of Stomatology, China Medical University, Shenyang, 110002, China 5 To whom correspondence should be addressed at Department of Periodontology, School of Stomatology, China Medical University, Shenyang, 110002, China.
synthesis, many by-products, such as reactive oxygen species (ROS), were generated. ROS are often regarded to be the major source of cellular damage. They play physiological roles when at normal levels; however, once they are excessively accumulated, they may initiate a cascade of oxidative damage of proteins, nucleic acids, and fatty acids, which leads to aging, neurodegeneration, metabolic disorders, cancer, and inflammatory diseases [2]. ROS are proposed to play a causative role in inducing mitochondrial dysfunction, while mitochondrial dysfunction, in turn, can increase the formation of ROS. Therefore, damaged mitochondria need to be cleared in time. Lemasters first termed such a selective removal process of mitochondria Bmitophagy^ [3], by
Data Loading...
