Reply to Voelkel: Cigarette Smoke is an Endothelial Cell Toxin
Year: 2017
Type: letter
Abstract: The report by Polverino and colleagues (1) provides a wonderful example of productive interdisciplinary collaboration.The authors connect lung and kidney endothelial cell damage and cigarette smoke in patients with chronic obstructive pulmonary disease and in smoke-exposed mice.This is an important study with far-reaching implications.Mechanistically, the authors point to generation of advanced glycation end products and receptor for advanced glycation end products activation triggered by oxidant stress, yet there are likely additional mechanisms that can be considered.Because the kidneys do not inhale, it is evident that it is the "circulating cigarette smoke" that is toxic to endothelial cells.For example, one component of cigarette smoke is the highly aggressive aldehyde acrolein (2-4), which can be measured in the blood and urine of smokers.A large number of experimental studies leave no doubt that cigarette smoke extract injures cultured endothelial cells.These findings have been frequently ignored or characterized as clinically irrelevant, yet they provide mechanistic insights and allow us to consider the hypothesis that emphysema is a vascular problem (5).If the notion that cigarette smoke cannot cross the alveolarcapillary barrier is dismissed, the fact that components of cigarette smoke are circulating has been firmly established.Although cigarette smoke extract in vitro kills endothelial cells directly, in vivo cigarette smoke components could, in susceptible individuals, trigger an immune response that includes the production of antiendothelial antibodies (6).Another implication of the findings published by Polverino and colleagues is that not only are the lung and kidney microvessels affected by cigarette smoke components but similarly the microcirculation of the skeletal muscles, the myocardium, and the retina are affected (1).Interesting correlations, not provided by the authors, are those between albuminuria and the diffusing capacity of the lung for carbon monoxide and albuminuria and urinary isoprostane concentration (7).Last, this study suggests that the vascular chronic obstructive pulmonary disease phenotype might benefit from antioxidant treatments.
Language: English
Subfield: Pulmonary and Respiratory Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W2738960269