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Cells 2018, 7(8), 86; https://doi.org/10.3390/cells7080086

Mitochondrial Quality Control in COPD and IPF

Division of Respiratory Diseases, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo 105-8461, Japan
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Received: 31 May 2018 / Revised: 6 July 2018 / Accepted: 24 July 2018 / Published: 24 July 2018
(This article belongs to the Special Issue Mitochondrial Biology in Health and Disease)
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Abstract

Mitochondria play important roles in the maintenance of intracellular homeostasis; hence, the quality control of mitochondria is crucial for cell fate determination. Mitochondria dynamics and mitochondria-specific autophagy, known as mitophagy, are two main quality control systems in cells. Mitochondria fuse to increase energy production in response to stress, and damaged mitochondria are segregated by fission and degraded by mitophagy. Once these systems are disrupted, dysfunctional mitochondria with decreased adenosine triphosphate (ATP) production and increased reactive oxygen species (ROS) production accumulate, affecting cell fate. Recently, increasing evidence suggests that the dysregulation of mitochondria quality control is pathogenic in several age-related diseases. In this review, we outlined the role of mitochondria quality control systems in the pathogenesis of age-associated lung diseases, chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF). View Full-Text
Keywords: mitochondria; mitochondria dynamics; mitophagy; chronic obstructive pulmonary disease (COPD); idiopathic pulmonary fibrosis (IPF) mitochondria; mitochondria dynamics; mitophagy; chronic obstructive pulmonary disease (COPD); idiopathic pulmonary fibrosis (IPF)
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).
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Hara, H.; Kuwano, K.; Araya, J. Mitochondrial Quality Control in COPD and IPF. Cells 2018, 7, 86.

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