2013
DOI: 10.1152/ajplung.00146.2013
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Abstract: Mitochondria are dynamic organelles that continuously change their shape through fission and fusion. Disruption of mitochondrial dynamics is involved in disease pathology through excessive reactive oxygen species (ROS) production. Accelerated cellular senescence resulting from cigarette smoke exposure with excessive ROS production has been implicated in the pathogenesis of chronic obstructive pulmonary disease (COPD). Hence, we investigated the involvement of mitochondrial dynamics and ROS production in terms … Show more

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Cited by 172 publications
(164 citation statements)
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“…24 In line with this observation, MitoTracker Red staining demonstrated that CSE induced depolarization of the mitochondrial membrane potential (Fig. 1A).…”
Section: Cse Induces Mitochondrial Ros Production and Cellular Senescsupporting
confidence: 75%
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“…24 In line with this observation, MitoTracker Red staining demonstrated that CSE induced depolarization of the mitochondrial membrane potential (Fig. 1A).…”
Section: Cse Induces Mitochondrial Ros Production and Cellular Senescsupporting
confidence: 75%
“…8,25 Hence, we assumed that our findings of accumulations of fragmented mitochondria might result from insufficient mitophagy in the airway epithelial cells of COPD lung and also in CSE-exposed HBEC. 8,24,25 Supporting this notion, autophagy and mitophagy activation induced by Torin1 resulted in enhanced degradation of autophagosomal contents including mitochondrial debris and an increase in undamaged mitochondrial number as shown by EM, and also reduced CSE-induced accumulation of ubiquitinated proteins and SQSTM1 in the mitochondrial fraction of HBEC (Fig. 2).…”
Section: Discussionmentioning
confidence: 57%
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