Īt the molecular level, many genes involved in cholesterol homeostasis and transport are expressed in the lungs, and in vitro and in vivo studies have demonstrated the importance of cholesterol homeostasis to lung physiology (reviewed in ). Increased HDL levels have also been reported in patients with severe COPD. Conversely, associations in the opposite direction were reported in the Multi- Ethnic Study of Atherosclerosis (MESA) study, in which HDL levels were negatively associated with FEV 1/FVC ratio and percent emphysema. Additionally, oxidized LDL levels were increased in COPD patients and were associated with lung function, inflammation, and oxidative stress. In the Third National Health and Nutrition Examination Survey (NHANES), forced expiratory volume in one second (FEV 1) was positively related to LDL and negatively related to HDL. A number of epidemiological studies reported significant correlations between serum lipids and lung function measures. Meta-analysis approaches have further supported the beneficial role of statins on outcomes among COPD patients. The endpoints in these studies included reductions in the rate of hospitalization, lung function decline, and death. Ī number of retrospective studies have shown that statins play a beneficial role in COPD. Statins are also reported to have pleiotropic effects including anti-inflammatory, anti-oxidant, anti-thrombogenic and neuroprotective properties. Statins reduce the risk of cardiovascular morbidities and mortality. Statins are widely used lipid-lowering agents that act through inhibiting 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, the rate-limiting step of hepatocyte cholesterol synthesis. COPD currently ranks as the fourth leading cause of death, and is predicted to become the third by 2020. This does not alter the authors’ adherence to PLOS ONE policies on sharing data and materials.Ĭhronic obstructive pulmonary disease (COPD) is characterized by chronic irreversible airflow limitation that is often accompanied by systemic inflammation and comorbidities. He has given lectures sponsored by BI and AZ. He has received research funding from AZ and Boehringer Ingelheim (BI). He has been a consultant with Amgen and Almirall. DDS: Over the past 3 years, DDS has served as a consultant on AstraZeneca (AZ) and Novartis Advisory Boards for COPD. Since Aughe as served as chief clinical scientist, new clinical development, AstraZeneca, UK. SR has served as a consultant, participated in advisory boards, received honorarium for speaking or grant support from: American Board of Internal Medicine, Advantage Healthcare, Almirall, American Thoracic Society, AstraZeneca, Baxter, Boehringer Ingelheim, Chiesi, ClearView Healthcare, Cleveland Clinic, Complete Medical Group, CSL, Dailchi Sankyo, Decision Resources, Forest, Gerson Lehman, Grifols, GroupH, Guidepoint Global, Haymarket, Huron Consulting, Inthought, Johnson and Johnson, Methodist Health System – Dallas, NCI Consulting, Novartis, Pearl, Penn Technology, Pfizer, PlanningShop, PSL FirstWord, Qwessential, Takeda, Theron and WebMD. The funder had no role in study design, data collection, analysis, interpretation or preparing the manuscript.Ĭompeting interests: BEM is an employee and shareholder of GSK. įunding: ECLIPSE study ( ) was funded by GlaxoSmithKline identifier NCT00292552 and GSK No. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are creditedĭata Availability: The raw expression data is available on the NCBI Gene Expression Omnibus (GEO) under accession number GSE71220. Received: Accepted: SeptemPublished: October 13, 2015Ĭopyright: © 2015 Obeidat et al. PLoS ONE 10(10):Įditor: Saeid Ghavami, University of Manitoba, CANADA (2015) The Effect of Statins on Blood Gene Expression in COPD. Citation: Obeidat M, Fishbane N, Nie Y, Chen V, Hollander Z, Tebbutt SJ, et al.
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