Chronic obstructive pulmonary disease (COPD) is one of the most common chronic respiratory diseases with high morbidity and mortality. It has become the fifth most burdened and the third most deadly disease in the global economy and increases year by year. The prevention and treatment of COPD are urgent. Smoking is the main and most common risk factor for COPD. Cigarette smoke (CS) contains a large number of toxic substances, can cause a series of changes in the trachea, lung tissue, pulmonary blood vessels, and promotes the occurrence and development of COPD. In recent years, the development of epigenetics and molecular biology have provided new guidance for revealing the pathogenesis, diagnosis, and treatment of diseases.
The latest research indicates that pulmonary vascular endothelial cell apoptosis initiates and participates in the pathogenesis of COPD (“The role of cigarette smoke-induced pulmonary vascular endothelial cell apoptosis in COPD” Qing Song et al. 2021).
There were studies found that in the systemic, cigarette smoke (CS) induced endothelial dysfunction through the following aspects: firstly, directed toxic efects of CS on endothelial cells; then, promoted the production of auto-antibodies in endothelial cells; next, CS-induced infammation of vascular; in addition, increased oxidative stress levels with reduced activation of the anti-oxidant pathways in endothelial cells; fnally, CS-induced increased mediators with vasoconstrictor, pro-infammatory, and remodelling activities and increased endoplasmic reticular stress and the unfolded protein response in endothelial cells (Wang Z et al. “Mitochon‑ drial fssion mediated cigarette smoke-induced pulmonary endothelial injury”. Am J Respir Cell Mol Biol. 2020).
Another recent study confirms the damage of smoking on skin (“Impact of cigarette smoke on physical-chemical and molecular proprieties of human skin in an ex vivo model”; Giuseppe Percoco et al. Exp. Dermatol. 2021). CS-induced oxidation of lipids at Human living skin explants (HSE) surface alters the skin barrier: interactions with polar products are enhanced and the lipid chain packing at the surface is modified. Consequently, skin permeability could increase which correlated with repression of CA9 and AQP1 genes.
Beside activation of AHR-NRF2 pathway in CS-exposed HSE, “our results suggested that mitochondrial functions were strongly impacted and oxidized lipids failed to be eliminated promoting skin barrier alteration”.
Smokers should use these scientific evidences to give up smoking.
Ex-smokers should consume dietary supplements containing natural antioxidants like hydroxytyrool to stimulate their internal defenses.
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