Modulation of oxidative stress and inflammatory burden is proposed as a novel therapeutic strategy to treat the pulmonary and systemic manifestations of COPD and comorbid cardiovascular disease.
This review highlights the shared inflammatory and oxidative stress pathways in COPD and atherosclerosis, suggesting these as targets for future dual-purpose therapeutics.
Abstract Chronic obstructive pulmonary disease (COPD) and atherosclerosis are chronic irreversible diseases, that share a number of common causative factors including cigarette smoking. Atherosclerosis drastically impairs blood flow and oxygen availability to tissues, leading to life-threatening outcomes including myocardial infarction (MI) and stroke. Patients with COPD are most likely to die as a result of a cardiovascular event, with 30% of all COPD-related deaths being attributed to cardiovascular disease (CVD). Both atherosclerosis and COPD involve significant local (i.e. lung, vasculature) and systemic inflammation and oxidative stress, of which current pharmacological treatments have limited efficacy, hence the urgency for the development of novel life-saving therapeutics. Currently these diseases must be treated individually, with no therapies available that can effectively reduce the likelihood of comorbid CVD other than cessation of cigarette smoking. In this review, the important mechanisms that drive atherosclerosis and CVD in people with COPD are explained and we propose that modulation of both the oxidative stress and the inflammatory burden will provide a novel therapeutic strategy to treat both the pulmonary and systemic manifestations related to these diseases.
Brassington et al. (Tue,) conducted a review in Chronic obstructive pulmonary disease (COPD) and atherosclerosis. Modulation of oxidative stress and inflammatory burden was evaluated. Modulation of oxidative stress and inflammatory burden is proposed as a novel therapeutic strategy to treat the pulmonary and systemic manifestations of COPD and comorbid cardiovascular disease.