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Related Concept Videos

Chronic Obstructive Pulmonary Disease II: Emphysema01:23

Chronic Obstructive Pulmonary Disease II: Emphysema

Emphysema, a major phenotype of chronic obstructive pulmonary disease (COPD), is characterized by irreversible destruction of alveolar walls and permanent enlargement of distal airspaces. Unlike chronic bronchitis, which primarily affects the airways, emphysema predominantly involves the lung parenchyma, where structural damage leads to airflow limitation.PathophysiologyIt most commonly results from prolonged exposure to cigarette smoke and other toxic gases, particularly cigarette smoke.
Chronic Obstructive Pulmonary Disease-II: Pathophysiology01:20

Chronic Obstructive Pulmonary Disease-II: Pathophysiology

Chronic Obstructive Pulmonary Disease (COPD) pathophysiology is intricate and multifaceted, involving a complex interplay of physiological processes. Understanding these mechanisms is crucial for effectively managing and treating COPD. Here is an in-depth look at the critical elements in the pathophysiology of COPD:
Chronic Inflammation
COPD: Pathogenesis and Clinical Features01:20

COPD: Pathogenesis and Clinical Features

Chronic obstructive pulmonary disease (COPD) is a group of lung conditions that progressively worsen over time, including chronic bronchitis and emphysema. This cluster of diseases collectively leads to a gradual and irreversible decline in lung function over time.
The primary cause for the onset of COPD is cigarette smoking and exposure to air pollution. These hazardous factors initiate a chain reaction within the lungs, resulting in chronic inflammation, damage to the airways, and a...
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Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features01:24

Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features

Chronic bronchitis is a key phenotype of chronic obstructive pulmonary disease (COPD), characterized by airway-centered inflammation and mucus overproduction. It develops from long-term exposure to harmful particles or gases, most commonly cigarette smoke, which triggers a persistent inflammatory response.Cellular and Structural ChangesInflammation initially affects the large bronchi and later the smaller airways, with infiltration by immune cells, including neutrophils, macrophages, and...
Chronic Obstructive Pulmonary Disease I: Introduction01:23

Chronic Obstructive Pulmonary Disease I: Introduction

Chronic obstructive pulmonary disease is a common, preventable, and treatable respiratory disorder characterized by persistent symptoms and progressive airflow limitation. This limitation results from a combination of small-airway disease (obstructive bronchiolitis) and parenchymal destruction (emphysema), both driven by chronic inflammation from exposure to harmful particles or gases.The disease includes two main pathological entities: emphysema, marked by destruction of alveolar walls and...

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Related Experiment Video

Updated: May 21, 2026

Standardized Measurement of Nasal Membrane Transepithelial Potential Difference (NPD)
09:47

Standardized Measurement of Nasal Membrane Transepithelial Potential Difference (NPD)

Published on: September 13, 2018

NFE2L2 pathway polymorphisms and lung function decline in chronic obstructive pulmonary disease.

Andrew J Sandford1, Deepti Malhotra, H Marike Boezen

  • 1UBC James Hogg Research Centre, Providence Heart + Lung Institute, St. Paul's Hospital, Vancouver, British Columbia, Canada. andrew.sandford@hli.ubc.ca

Physiological Genomics
|June 14, 2012
PubMed
Summary

Genetic variations in the Nuclear Erythroid 2-related factor 2 (NRF2) pathway do not appear to influence the rate of lung function decline in smokers. This study found no consistent replication of initial associations in a second cohort.

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Phenotyping Mouse Pulmonary Function In Vivo with the Lung Diffusing Capacity
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Last Updated: May 21, 2026

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09:47

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Published on: September 13, 2018

Phenotyping Mouse Pulmonary Function In Vivo with the Lung Diffusing Capacity
07:13

Phenotyping Mouse Pulmonary Function In Vivo with the Lung Diffusing Capacity

Published on: January 6, 2015

Area of Science:

  • Pulmonary Medicine
  • Genetics
  • Environmental Health

Background:

  • Oxidant-antioxidant imbalance is implicated in chronic obstructive pulmonary disease (COPD) development.
  • The Nuclear erythroid 2-related factor 2 (NRF2) pathway is crucial for lung defense against oxidants.
  • Genetic and environmental factors interact to cause COPD.

Purpose of the Study:

  • To investigate if polymorphisms in the NRF2 pathway genes affect the rate of lung function decline in smokers.
  • To validate findings in two independent cohorts: the Lung Health Study (LHS) and the Vlagtwedde-Vlaardingen cohort.

Main Methods:

  • Genotyping of polymorphisms in genes regulating or regulated by NRF2.
  • Statistical analysis to assess the association between NRF2 pathway gene polymorphisms and lung function decline rate.
  • Replication analysis in an independent cohort.

Main Results:

  • Several polymorphisms in 11 genes within the NRF2 pathway showed nominal significance for lung function decline in the LHS.
  • A polymorphism in KEAP1 (rs11085735) was associated with lung function level but not decline in the replication cohort.
  • Only one polymorphism in FOSL1 (rs634534) showed replication for lung function decline rate, but with inconsistent directionality.

Conclusions:

  • Despite initial associations in the LHS, polymorphisms in the NRF2 pathway genes did not show consistent replication for affecting lung function decline rate.
  • The findings suggest that variations in the NRF2 pathway may not be a significant predictor of lung function decline in smokers.