Abstract
Exposure of the airways epithelium to environmental insults, including cigarette smoke, results in increased oxidative stress due to unbalance between oxidants and antioxidants in favor of oxidants. Oxidative stress is a feature of inflammation and promotes the progression of chronic lung diseases, including Chronic Obstructive Pulmonary Disease (COPD). Increased oxidative stress leads to exhaustion of antioxidant defenses, alterations in autophagy/mitophagy and cell survival regulatory mechanisms, thus promoting cell senescence. All these events are amplified by the increase of inflammation driven by oxidative stress. Several models of bronchial epithelial cells are used to study the molecular mechanisms and the cellular functions altered by cigarette smoke extract (CSE) exposure, and to test the efficacy of molecules with antioxidant properties. This review offers a comprehensive synthesis of human in-vitro and ex-vivo studies published from 2011 to 2021 describing the molecular and cellular mechanisms evoked by CSE exposure in bronchial epithelial cells, the most used experimental models and the mechanisms of action of cellular antioxidants systems as well as natural and synthetic antioxidant compounds.
Highlights
IntroductionIncreased oxidative stress leads to exhaustion of antioxidant defenses, alterations in autophagy/mitophagy and cell survival regulatory mechanisms, promoting cell senescence
This review summarizes our current understanding of the impact of increased oxidative stress in human bronchial epithelial cells exposed to cigarette smoke extract (CSE)
Exclusion criteria were: (1) animal-only studies; (2) studies without cellular models; (3) studies focusing on exposure to electronic-cigarette smoke or studies where cells were stimulated with single tobacco components; (4) studies focusing on cancer cells, alveolar cells, or epithelial cells from other organs; (5) papers out of topic; (6) case reports, reviews, or conference abstracts
Summary
Increased oxidative stress leads to exhaustion of antioxidant defenses, alterations in autophagy/mitophagy and cell survival regulatory mechanisms, promoting cell senescence. All these events are amplified by the increase of inflammation driven by oxidative stress. Several models of bronchial epithelial cells are used to study the molecular mechanisms and the cellular functions altered by cigarette smoke extract (CSE) exposure, and to test the efficacy of molecules with antioxidant properties. Cigarette smoke (CS), the main risk factor for COPD, alters airway epithelial barrier function and increases oxidative stress promoting senescence and activation of proinflammatory pathways in the airway epithelium [2].
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