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. 2022 Jul 11;19:10. doi: 10.1186/s12950-022-00308-9

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© The Author(s) 2022

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — Sources of reactive oxidant species (ROS) within the lung. The high levels of ROS reported in the lung and airways of COPD subjects is derived from both exogenous and exogenous sources. Exogenous sources include cigarette smoking, environmental pollution, pathogens and inflammation. ROS is generated endogenously through mitochondria including mitochondrial ROS (mtROS), peroxisome activation, hypoxia and inflammation. ROS affects the function of many intracellular organelles such as proteasome, inflammasome, lysosome and the endoplasmic reticulum (ER) via the unfolded protein response (UPR) to elicit detrimental effects on cellular functions