Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Few smokers develop COPD. Why?

N M Siafakas1, E G Tzortzaki

  • 1Department of Thoracic Medicine, University of Crete, Medical School, Heraklion, Crete, Greece. siafak@med.uoc.gr

Respiratory Medicine
|August 28, 2002
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Combined Pulmonary Fibrosis and Emphysema in Scleroderma-Related Lung Disease Has a Major Confounding Effect on Lung Physiology and Screening for Pulmonary Hypertension.

Arthritis & rheumatology (Hoboken, N.J.)·2015
Same author

Stability of phenotypes defined by physiological variables and biomarkers in adults with asthma.

Allergy·2014
Same author

Differential telomerase expression in idiopathic pulmonary fibrosis and non-small cell lung cancer.

Oncology reports·2013
Same author

An update on idiopathic pulmonary fibrosis.

Panminerva medica·2013
Same author

The presence of Merkel cell polyomavirus is associated with deregulated expression of BRAF and Bcl-2 genes in non-small cell lung cancer.

International journal of cancer·2013
Same author

Recent advances in the pathogenesis and clinical evaluation of pulmonary fibrosis.

European respiratory review : an official journal of the European Respiratory Society·2012
Same journal

Prediction of therapeutic effect of antifibrotic therapy for idiopathic pulmonary fibrosis using quantitative CT texture analysis.

Respiratory medicine·2026
Same journal

Obesity and Early Sepsis-Associated Acute Respiratory Distress Syndrome: A Prospective Multicenter Study.

Respiratory medicine·2026
Same journal

Adults with Congenital Lung Malformations: A Descriptive Analysis of an Underexplored Population.

Respiratory medicine·2026
Same journal

Risk Factors and Microbiological Characteristics of Ventilator-Associated Pneumonia in a Tunisian Intensive Care Unit During the COVID-19 Pandemic.

Respiratory medicine·2026
Same journal

Impact of Therapeutic Hypothermia on Oxygen Demand and Respiratory Function in Post-Cardiac Arrest Patients: A Retrospective Cohort Study.

Respiratory medicine·2026
Same journal

The longitudinal decrease in exercise tolerance and disease progression in mild-to-moderate COPD.

Respiratory medicine·2026
See all related articles

Only a minority of smokers develop COPD. Susceptibility is likely due to genetic factors interacting with environmental exposures, influencing inflammation and tissue damage pathways in chronic obstructive pulmonary disease.

Area of Science:

  • Pulmonary Medicine
  • Genetics
  • Environmental Health

Background:

  • Chronic obstructive pulmonary disease (COPD) is a major health concern, primarily linked to cigarette smoking.
  • Despite smoking being the main risk factor, only a subset of smokers develop clinically significant COPD, indicating host susceptibility.
  • The pathogenesis involves abnormal inflammation, oxidative stress, tissue damage, and remodeling, but pathways remain incompletely understood.

Purpose of the Study:

  • To review the available literature on factors contributing to susceptibility in smokers who develop COPD.
  • To explore epidemiological, environmental, and genetic factors influencing COPD development.
  • To identify potential genetic markers for COPD susceptibility.

Main Methods:

  • Literature review of epidemiological, environmental, and genetic studies related to COPD pathogenesis.

Related Experiment Videos

  • Discussion of an epidemiological model emphasizing timing of smoke exposure.
  • Review of candidate genes and genetic alterations associated with COPD.

    • Main Results:

    • Early-life respiratory adenoviral infections and nutritional differences may influence COPD risk.
    • Airway hyperresponsiveness alone does not fully explain susceptibility.
    • Genetic factors are the most probable explanation for 'susceptible' smokers, with alpha-1-antitrypsin deficiency being the primary established genetic risk factor.
    • Several other candidate genes and microsatellite DNA instability show potential relevance.

    Conclusions:

    • COPD development is multifactorial, involving both exogenous exposures (like smoking) and endogenous host factors.
    • Genetic predisposition, likely involving multiple genes, plays a crucial role in determining individual susceptibility to COPD.
    • Further research into genetic alterations and their interaction with environmental factors is needed to fully elucidate COPD pathogenesis.