Geroprotectors as a Novel Therapeutic Strategy for COPD, an Accelerating Aging Disease – Published by Dove Medical Press
A new way of looking at COPD and the Aging Lung
London, United Kingdom (PRWEB) September 25, 2012
International Journal of Chronic Obstructive Pulmonary Disease (IJCOPD), published by Dove Medical Press, will highlight one of its most recently published articles: “Geroprotectors as a novel therapeutic strategy for COPD, an accelerating aging disease.”
According to Dr. Richard E Russell, IJCOPD Editor-in-Chief, “This excellent review summarises a new way of looking at COPD and the aging lung. This is going to be an area of greatly increased interest and insights gained may lead to breakthroughs in many inflammatory and age related degenerative conditions.”
The lung is normally aged but exposure to environmental factors such as tobacco smoke causes accelerating aging of lungs,” explains Dr. Ito Kazuhiro, author. “This causes an increased risk of respiratory infection, lung cancer and chronic obstructive pulmonary disease (COPD) where effective treatment is not available.” Dr. Kazuhiro’s review provides the molecular mechanism of COPD as accelerating aging lung disease and future prospect of anti- aging strategy, called geroprotector for the treatment of COPD.
Chronic obstructive pulmonary disease (COPD) progresses very slowly and the majority of patients are therefore elderly. COPD is characterized by an abnormal persistent inflammatory response to noxious environmental stimuli and there are increasing evidences for a close relationship between premature aging and chronic inflammatory diseases. Thus, COPD is considered to be a disease of an accelerating aging.
The authors collected the evidence for roles of aging on pathogenesis of COPD and considered future therapeutic strategy for COPD based on this senescence hypothesis. Since calorie restriction has been proved to extend lifespan, many efforts were made to clarify the molecular mechanism of aging. Aging is defined as the progressive decline of homeostasis that occurs after the reproductive phase of life is complete, leading to an increasing risk of disease or death due to impaired DNA repair after damage by oxidative stress or telomere shortening as a result of repeated cell division.
During aging, pulmonary function progressively deteriorates; innate immunity is impaired and pulmonary inflammation increases, accompanied by structural changes, such as an enlargement of airspaces. Noxious environmental gases, such as cigarette smoke, may worsen these aging-related events in the lung or accelerate aging of the lung due to reduction in anti-aging molecules and/or stimulation of aging molecules.
Aging signaling are complex but conserved in divert species, such as worm, fruit fry, rodent and humans. Especially the insulin like growth factor (IGF-1) signaling was well documented. Geroprotectors are therapeutics that affect the root cause of aging and age-related diseases, and thus prolong the life-span of animals. Most of geroprotectors such as melatonin, metformin, rapamycin and resveratrol are anti-oxidant or anti-aging molecule regulators. Therefore, geroprotection for the lung might be an attractive approach for the treatment of COPD by preventing premature aging of lung.
The authors of the article are as follows: Kazuhir Ito, Thomas Colley, Nicolas Mercado, Airways Disease Section, National Heart and Lung Institute, Imperial College London, UK.
IJCOPD is an international, peer-reviewed journal of therapeutics and pharmacology focusing on concise rapid reporting of clinical studies and reviews in COPD. Special focus will be given to the pathophysiological processes underlying the disease, intervention programs, patient focused education, and self management protocols. This journal is directed at specialists and healthcare professionals.
Dove Medical Press Ltd is a privately held company specializing in the publication of Open Access peer-reviewed journals across the broad spectrum of science, technology and especially medicine.
For the original version on PRWeb visit: http://www.prweb.com/releases/prweb2012/9/prweb9793049.htm