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Animal models and mechanisms of tobacco smoke-induced chronic obstructive pulmonary disease (COPD)

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Chronic obstructive pulmonary disease (COPD) is the third leading cause of death worldwide, and its global health burden is increasing. COPD is characterized by emphysema, mucus hypersecretion, and persistent lung inflammation, and clinically presented with chronic airflow obstruction and symptoms of dyspnea and fatigue in patients. A cluster of pathologies including chronic bronchitis, emphysema, asthma, and cardiovascular disease in the form of hypertension and atherosclerosis variably coexist in COPD patients. Underlying causes for COPD are primarily due to tobacco use but may also be driven by air pollution, biomass burning, and workplace related fumes and chemicals. While no single animal model can mimic all features of human COPD, the wide variety of models studied in the literature have collectively helped to improve our understanding of those disease processes involved in the genesis and persistence of COPD. In this review, the pathogenesis and associated risk factors of COPD are in relation to different mammalian models of the disease. Each animal model included in this review is exclusively created by tobacco smoke (TS) exposure. As animal models continue to aid in defining the pathobiological mechanisms of and possible novel therapeutic interventions for COPD, the advantages and disadvantages of each animal model are discussed.

Impact/Purpose

This review paper discusses the current understanding of the Chronic Obstructive Pulmonary Disease (COPD) pathobiology and use of animal models. The current global burden of COPD is substantial, and the prevalence of this devastating disease is rising. Multiple rational models for human COPD have been developed (Table 1), and they are essential to the study of TS-induced lung disfunction, diseases, and pathologies related to COPD (Table 2). Significant progress has been made in our understanding of the biological mechanisms of COPD, specifically the role of macrophage phenotypes, lymphocyte subpopulations, and protease/antiprotease defense mechanisms. However, the key factors contributing to the progression of inflammation and exacerbation of COPD remain unclear.

Citation

Upadhyay, P., C. Wu, A. Pham, A. Zeki, C. Royer, U. Kodavanti, M. Takeuchi, H. Bayram, AND K. Pinkerton. Animal models and mechanisms of tobacco smoke-induced chronic obstructive pulmonary disease (COPD). Taylor & Francis, Inc., Philadelphia, PA, 26(5):275-305, (2023). [DOI: 10.1080/10937404.2023.2208886]

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DOI: Animal models and mechanisms of tobacco smoke-induced chronic obstructive pulmonary disease (COPD)
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Last updated on December 12, 2024
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