Related Experiment Video
Updated: Feb 17, 2026
09:50
Impact Assessment of Repeated Exposure of Organotypic 3D Bronchial and Nasal Tissue Culture Models to Whole Cigarette Smoke
Published on: February 12, 2015
11.7K
Genetic Pleiotropy between Nicotine Dependence and Respiratory Outcomes
Jushan Zhang1,2, Shouneng Peng3,4, Haoxiang Cheng3,4
1Department of Respiratory Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai 200072, China.
Scientific Reports
|December 6, 2017
Summary
Genetic predisposition to nicotine dependence influences chronic obstructive pulmonary disease (COPD) risk and lung function independently of smoking behavior. This genetic pleiotropy suggests direct effects on respiratory health beyond smoking habits.
Area of Science:
- Genetics
- Respiratory Medicine
- Public Health
Background:
- Smoking is a primary cause of respiratory diseases, including chronic obstructive pulmonary disease (COPD).
- The genetic links between smoking behaviors and lung health outcomes like COPD have not been fully elucidated.
- Genetic pleiotropy, where a single gene influences multiple traits, is a potential factor.
Purpose of the Study:
- To investigate the genetic pleiotropy between smoking behavior and lung function/COPD.
- To determine if genetic predisposition to nicotine dependence affects COPD risk and lung function.
- To explore whether the genetic influence follows a causal or independent model.
Main Methods:
- Utilized large-scale genetic datasets for smoking behavior, lung function, and COPD.
- Performed genetic association analyses to examine the relationship between nicotine dependence loci and COPD risk/lung function.
- Adjusted for smoking behavior to differentiate direct genetic effects from smoking-mediated effects.
Main Results:
- Genetic predisposition to nicotine dependence is associated with increased COPD risk, independent of smoking behavior.
- Specific nicotine dependence loci (15q25.1 and 19q13.2) are linked to lung function, even after adjusting for smoking.
- Significant overlap in genetic association signals between lung function and smoking parameters (cigarettes per day, former smoking) was observed.
- Empirical data support genetic pleiotropy between nicotine dependence and COPD/lung function, often acting through an independent model.
Conclusions:
- Genetic factors influencing nicotine dependence have a direct impact on COPD risk and lung function, separate from their effect on smoking intensity.
- The genetic pleiotropy between nicotine dependence and respiratory health is complex, involving numerous variants acting independently.
- These findings highlight novel genetic pathways contributing to respiratory diseases in smokers.
More Related Videos
Related Concept Videos
01:23Drugs Acting on Autonomic Ganglia: Stimulants
2.1K
Ganglionic stimulants activate NM nicotinic receptors in autonomic ganglia, falling into two categories: nicotine mimetics [e.g., lobeline, dimethylpiperazine, tetramethylammonium] and muscarinic receptor agonists [e.g., muscarine, methacholine]. The first category's action is rapid and blocked by nicotinic receptor antagonists, while the second category's action is delayed and blocked by atropine-like agents. Nicotine, an alkaloid, affects the heart rate by stimulating...
2.1K
01:11Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase
18
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...
18
01:29Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu
10
Genetic variations significantly influence drug response through pharmacokinetics, receptor interactions, and biologic milieu modifications. Pharmacokinetic alterations impact drug metabolism and clearance, affecting efficacy and toxicity. Variants in drug-metabolizing enzymes, such as CYP2C9 and CYP2C19, alter drug activation and elimination. For example, CYP2C9 loss-of-function variants require lower warfarin doses to prevent excessive bleeding, while CYP2C19 variants reduce clopidogrel...
10
01:20Chronic Obstructive Pulmonary Disease-II: Pathophysiology
4.8K
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
Chronic Inflammation
4.8K
01:28Human Genetics
1.7K
Human genetics provides a profound framework for understanding the interplay between genetic predispositions and human psychology. At the heart of this discipline lies the study of how genes influence physical traits, behaviors, and susceptibility to diseases. Each person carries a unique genetic code that subtly or significantly shapes their psychological and behavioral landscape.
The complex relationship between genetics and psychology is observable through common biological components such...
The complex relationship between genetics and psychology is observable through common biological components such...
1.7K
01:20COPD: Pathogenesis and Clinical Features
1.9K
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...
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...
1.9K