Han 2019 Am J Respir Cell Mol Biol

Han S, Chandel NS (2019) There is no smoke without mitochondria. Am J Respir Cell Mol Biol 60:489-91. https://doi.org/10.1165/rcmb.2018-0348ED

» PMID: 30383397 Open Access

Han S, Chandel NS (2019) Am J Respir Cell Mol Biol

Abstract: Mitochondria have been increasingly recognized as a contributing factor to the pathogenesis of chronic obstructive pulmonary disease (COPD). Patients with COPD manifest chronic airway inflammation and progressive destruction of alveolar structures. Multiple factors are believed to be involved in the development of COPD, including increased levels of reactive oxygen species (ROS), protease–antiprotease imbalance, exaggerated inflammation, cell apoptosis/death, and accelerated cellular senescence. Changes in the mitochondrial respiratory chain complexes and ROS levels also have been implicated in the development of COPD. For example, airway smooth muscle cells cultured from patients with COPD have a reduced expression of complexes I, III, and V; increased mitochondrial ROS; and decreased membrane potential and ATP production (1).

• Bioblast editor: Gnaiger E

Correction: FADH₂ and Complex II

FADH₂ is shown as the substrate feeding electrons into Complex II (CII). This is wrong and requires correction - for details see Gnaiger (2024).

Gnaiger E (2024) Complex II ambiguities ― FADH₂ in the electron transfer system. J Biol Chem 300:105470. https://doi.org/10.1016/j.jbc.2023.105470 - »Bioblast link«

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Enzyme: Complex II;succinate dehydrogenase