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Cigarette smoke-induced proteostasis imbalance in obstructive lung diseases
1Respiratory Division, Department of Medicine, Centre Hospitalier Universitaire de Sherbrooke, Quebec, Canada. Andre.Cantin@USherbrooke.ca
Current Molecular Medicine
|June 16, 2012
Summary
Cigarette smoke overwhelms lung cells, but the unfolded protein response (UPR) helps maintain proteostasis and prevent chronic obstructive pulmonary disease (COPD). This cellular defense mechanism combats oxidative stress and ER stress, promoting cell survival.
Area of Science:
- Pulmonary Medicine
- Cellular Biology
- Toxicology
Background:
- The lungs face daily exposure to oxidants from air pollution and smoking.
- Cigarette smoke significantly increases the burden of reactive oxidants, risking lung cell damage.
- Oxidative stress can disrupt proteostasis, the regulation of protein synthesis, folding, and turnover.
Purpose of the Study:
- To review mechanisms of healthy and dysfunctional proteostasis in the context of cigarette smoke exposure.
- To explore the role of the unfolded protein response (UPR) in mitigating cigarette smoke-induced cellular stress.
- To understand how these processes relate to the development of chronic obstructive pulmonary disease (COPD).
Main Methods:
- Review of existing literature on cellular responses to oxidative stress.
- Analysis of signaling pathways involved in the unfolded protein response (UPR).
- Examination of the transcription factor Nrf2's role in antioxidant gene expression.
Main Results:
- Most chronic smokers do not develop COPD due to a highly effective UPR.
- UPR activation reduces endoplasmic reticulum (ER) stress by decreasing protein translation and increasing protein degradation.
- UPR enhances cell survival through mechanisms like chaperone-mediated protein folding and Nrf2-induced antioxidant gene expression.
Conclusions:
- The unfolded protein response (UPR) is crucial for maintaining proteostasis and cell survival against cigarette smoke-induced oxidative and ER stress.
- Dysfunctional proteostasis can lead to apoptosis, potentially contributing to COPD development.
- Understanding these mechanisms offers insights into preventing and treating smoking-related lung diseases.
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