Chronic obstructive pulmonary disease. Mechanisms of disease development and prevention strategies with antioxidants.
Oxygen/Nitrogen Radicals: Lung Injury and Disease (Lung Biology in Health and Disease). Vol. 187. New York: Marcel Dekker, 2004 Apr; 187:361-391
To summarize, one can say with certainty that COPD develops in genetically susceptible individuals after prolonged exposure to cigarette smoke. Presently, most of the genes contributing to this are unknown. Alpha1-A T deficiency is a risk factor for COPD, but other genetic associations with this disease must still be considered as tentative. The key to establishing that a gene modifies the risk for a disease is replication of the association in different populations. This is a difficult task. Besides alpha1-AT, only the GST-Ml, VDBP, and CFTR genes have been implicated as risk factors in more than one population. Identification of other candidate genes would further enhance the understanding of COPD pathogenesis at the molecular level. There is also good evidence that the propensity to smoke cigarettes and the likelihood of quitting smoking are influenced by genetic factors. This can be useful in efforts directed at cessation of smoking. The responses to hypoxia and hypercapnia also seem to be influenced by genetic factors. Identification of the genes involved could yield important insights into the pathogenesis of COPD and provide new targets for therapeutic interventions for this debilitating disease.
Antioxidants; Antioxidation; Carcinogenesis; Respiratory-system-disorders; Pulmonary-system-disorders; Lung-disease; Lung-disorders; Lung-function; Pulmonary-function; Chronic-degenerative-diseases; Cigarette-smoking; Tobacco-smoke
Book or book chapter
Vallyathan-V; Castranova-V; Shi-X
Research Tools and Approaches: Cancer Research Methods
Oxygen/Nitrogen Radicals: Lung Injury and Disease (Lung Biology in Health and Disease)