Priya Upadhyay, Ching-Wen Wu, Alexa Pham, Amir A Zeki, Christopher M Royer, Urmila P Kodavanti, Minoru Takeuchi, Hasan Bayram, Kent E Pinkerton
{"title":"烟草烟雾引起的慢性阻塞性肺疾病(COPD)的动物模型和机制。","authors":"Priya Upadhyay, Ching-Wen Wu, Alexa Pham, Amir A Zeki, Christopher M Royer, Urmila P Kodavanti, Minoru Takeuchi, Hasan Bayram, Kent E Pinkerton","doi":"10.1080/10937404.2023.2208886","DOIUrl":null,"url":null,"abstract":"<p><p>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 by chronic airflow obstruction and symptoms of dyspnea, cough, 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 include primarily tobacco use but may also be driven by exposure to air pollutants, biomass burning, and workplace related fumes and chemicals. While no single animal model might mimic all features of human COPD, a wide variety of published models have collectively helped to improve our understanding of disease processes involved in the genesis and persistence of COPD. In this review, the pathogenesis and associated risk factors of COPD are examined in 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.</p>","PeriodicalId":49971,"journal":{"name":"Journal of Toxicology and Environmental Health-Part B-Critical Reviews","volume":"26 5","pages":"275-305"},"PeriodicalIF":6.4000,"publicationDate":"2023-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10718174/pdf/","citationCount":"0","resultStr":"{\"title\":\"Animal models and mechanisms of tobacco smoke-induced chronic obstructive pulmonary disease (COPD).\",\"authors\":\"Priya Upadhyay, Ching-Wen Wu, Alexa Pham, Amir A Zeki, Christopher M Royer, Urmila P Kodavanti, Minoru Takeuchi, Hasan Bayram, Kent E Pinkerton\",\"doi\":\"10.1080/10937404.2023.2208886\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>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 by chronic airflow obstruction and symptoms of dyspnea, cough, 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 include primarily tobacco use but may also be driven by exposure to air pollutants, biomass burning, and workplace related fumes and chemicals. While no single animal model might mimic all features of human COPD, a wide variety of published models have collectively helped to improve our understanding of disease processes involved in the genesis and persistence of COPD. In this review, the pathogenesis and associated risk factors of COPD are examined in 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.</p>\",\"PeriodicalId\":49971,\"journal\":{\"name\":\"Journal of Toxicology and Environmental Health-Part B-Critical Reviews\",\"volume\":\"26 5\",\"pages\":\"275-305\"},\"PeriodicalIF\":6.4000,\"publicationDate\":\"2023-07-04\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10718174/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Toxicology and Environmental Health-Part B-Critical Reviews\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1080/10937404.2023.2208886\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2023/5/14 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q1\",\"JCRName\":\"ENVIRONMENTAL SCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Toxicology and Environmental Health-Part B-Critical Reviews","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/10937404.2023.2208886","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2023/5/14 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"ENVIRONMENTAL SCIENCES","Score":null,"Total":0}
Animal models and mechanisms of tobacco smoke-induced chronic obstructive pulmonary disease (COPD).
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 by chronic airflow obstruction and symptoms of dyspnea, cough, 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 include primarily tobacco use but may also be driven by exposure to air pollutants, biomass burning, and workplace related fumes and chemicals. While no single animal model might mimic all features of human COPD, a wide variety of published models have collectively helped to improve our understanding of disease processes involved in the genesis and persistence of COPD. In this review, the pathogenesis and associated risk factors of COPD are examined in 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.
期刊介绍:
"Journal of Toxicology and Environmental Health: Part B - Critical Reviews" is an academic journal published by Taylor & Francis, focusing on the critical examination of research in the areas of environmental exposure and population health. With an ISSN identifier of 1093-7404, this journal has established itself as a significant source of scholarly content in the field of toxicology and environmental health.
Since its inception, the journal has published over 424 articles that have garnered 35,097 citations, reflecting its impact and relevance in the scientific community. Known for its comprehensive reviews, the journal also goes by the names "Critical Reviews" and "Journal of Toxicology & Environmental Health, Part B, Critical Reviews."
The journal's mission is to provide a platform for in-depth analysis and critical discussion of the latest findings in toxicology, environmental health, and related disciplines. By doing so, it contributes to the advancement of knowledge and understanding of the complex interactions between environmental factors and human health, aiding in the development of strategies to protect and improve public health.