ArticleFrontiers in physiology2013
Tobacco smoke induced COPD/emphysema in the animal model-are we all on the same page?
Article in Frontiers in physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 87 citations in OpenAlex.
- Molecular and Cellular Mechanisms Responsible for Beneficial Effects of Mesenchymal Stem Cell-Derived Product "Exo-d-MAPPS" in Attenuation of Chronic Airway Inflammation.Analytical cellular pathology (Amsterdam) · 2020Trial
- Efficacy of a hydrogen-oxygen generator in treating cigarette smoke-induced chronic obstructive pulmonary disease in rats.Current research in toxicology · 2025Article
- Cigarette smoke exposure impairs early-stage recovery from lengthening contraction-induced muscle injury in male mice.Physiological reports · 2024Article
- Baicalin Relieves Airway Inflammation in COPD by Inhibiting miR-125a.Applied biochemistry and biotechnology · 2024Article
- Rieske Iron-Sulfur Protein Mediates Pulmonary Hypertension Following Nicotine/Hypoxia Coexposure.American journal of respiratory cell and molecular biology · 2024Article
- Review
- Animal models: An essential tool to dissect the heterogeneity of chronic obstructive pulmonary disease.Journal of translational internal medicine · 2023Article
- Ginseng Saponin Rb1 Attenuates Cigarette Smoke Exposure-Induced Inflammation, Apoptosis and Oxidative Stress via Activating Nrf2 and Inhibiting NF-κB Signaling Pathways.International journal of chronic obstructive pulmonary disease · 2023Article
- The importance of vascular epithelial growth factor (VEGF) and inducible nitric oxide synthase (INOS) in rhinitis medicamentosa pathogenesis: An experimental rat model study.Histology and histopathology · 2022Article
- Preventive effect of total flavonoids ofAnnals of translational medicine · 2022Article
- Gene Expression Trajectories from Normal Nonsmokers to COPD Smokers and Disease Progression Discriminant Modeling in Response to Cigarette Smoking.Disease markers · 2022Article
- A 6-month inhalation toxicology study in ApoeArchives of toxicology · 2021Article
- Long-term electronic cigarette exposure induces cardiovascular dysfunction similar to tobacco cigarettes: role of nicotine and exposure duration.American journal of physiology. Heart and circulatory physiology · 2021Article
- Dynamic evolution of emphysema and airway remodeling in two mouse models of COPD.BMC pulmonary medicine · 2021Article
- Human umbilical cord mesenchymal stem cell-derived extracellular vesicles ameliorate airway inflammation in a rat model of chronic obstructive pulmonary disease (COPD).Stem cell research & therapy · 2021Article
- Macrophages Inhibit Ciliary Protein Levels by Secreting BMP-2 Leading to Airway Epithelial Remodeling Under Cigarette Smoke Exposure.Frontiers in molecular biosciences · 2021Article
- Cerebrovascular and Neurological Dysfunction under the Threat of COVID-19: Is There a Comorbid Role for Smoking and Vaping?International journal of molecular sciences · 2020Review
- Immunomodulatory Effects of Hydrolyzed Seawater Pearl Tablet (HSPT) on Th1/Th2 Functionality in a Mice Model of Chronic Obstructive Pulmonary Disease (COPD) Induced by Cigarette Smoke.Evidence-based complementary and alternative medicine : eCAM · 2020Review
- Animal Models Reflecting Chronic Obstructive Pulmonary Disease and Related Respiratory Disorders: Translating Pre-Clinical Data into Clinical Relevance.Journal of innate immunity · 2020Review
- Animal models of emphysema.Chinese medical journal · 2019Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic Obstructive Pulmonary Disease (COPD) is one of the foremost causes of death worldwide. It is primarily caused by tobacco smoke, making it an easily preventable disease, but facilitated by genetic α-1 antitrypsin deficiency. In addition to active smokers, health problems also occur in people involuntarily exposed to second hand smoke (SHS). Currently, the relationship between SHS and COPD is not well established. Knowledge of pathogenic mechanisms is limited, thereby halting the advancement of new treatments for this socially and economically detrimental disease. Here, we attempt to summarize tobacco smoke studies undertaken in animal models, applying both mainstream (direct, nose only) and side stream (indirect, whole body) smoke exposures. This overview of 155 studies compares cellular and molecular mechanisms as well as proteolytic, inflammatory, and vasoreactive responses underlying COPD development. This is a difficult task, as listing of exposure parameters is limited for most experiments. We show that both mainstream and SHS studies largely present similar inflammatory cell populations dominated by macrophages as well as elevated chemokine/cytokine levels, such as TNF-α. Additionally, SHS, like mainstream smoke, has been shown to cause vascular remodeling and neutrophil elastase-mediated proteolytic matrix breakdown with failure to repair. Disease mechanisms and therapeutic interventions appear to coincide in both exposure scenarios. One of the more widely applied interventions, the anti-oxidant therapy, is successful for both mainstream and SHS. The comparison of direct with indirect smoke exposure studies in this review emphasizes that, even though there are many overlapping pathways, it is not conclusive that SHS is using exactly the same mechanisms as direct smoke in COPD pathogenesis, but should be considered a preventable health risk. Some characteristics and therapeutic alternatives uniquely exist in SHS-related COPD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.