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Figure 1. Mitochondrial perspective of chronic obstructive pulmonary disease (COPD) pathogenesis. Nucleotide binding domain and leucine-rich-repeat-containing protein X1 (NLRX1), which might have a crucial inhibitory role to keep alveolar macrophages (AMs) in a quiescent homeostatic status, is suppressed in patients with COPD. The suppression of NLRX1 in AMs is associated with mitochondrial dysfunction and leads to the increase of inflammasome activation, protease burden as well as production of mitochondrial reactive oxygen species (ROS), which culminate in the development of COPD. CS: cigarette smoke; IL-18: interleukin 18; MMP: matrix metalloproteinase. Please see the main text for the explanation in detail. Modified from Yoon CM, et al. J Innate Immun 2016;8:121-8, with permission of S. Karger AG, Basel.. From: A Mitochondrial Perspective of Chronic Obstructive Pulmonary Disease Pathogenesis.
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