Abstract
BackgroundTo systematically analyze the influence of genetic polymorphisms of matrix metalloproteinase 9 (MMP9) on susceptibility to chronic obstructive pulmonary disease (COPD).MethodsRelevant literatures reporting MMP9 and susceptibility to COPD in PubMed, Web of Science, VIP, Wanfang and CNKI databases were searched using the key words "matrix metalloproteinases 9/MMP9, COPD/chronic obstructive pulmonary disease". Data of eligible literatures were extracted and analyzed for the odds ratio (OR) and corresponding 95% CI.ResultsA total of 16 independent studies reporting MMP9-1562C/T and COPD patients were enrolled and analyzed. None of the genetic models revealed the relationship between MMP9-1562C/T and susceptibility to COPD. Subgroup analyses identified lower risk of COPD in Chinese population carrying the TT genotype for theMMP9 rs3918242 relative to those carrying CT and CC genotypes (P=0.03, OR=0.67, 95% CI=0.46-0.97).ConclusionsChinese population carrying the TT genotype for the MMP-9 rs3918242 present lower susceptibility to COPD relative to those carrying CT and CC genotypes.
Highlights
Chronic obstructive pulmonary disease (COPD) is a worldwide disease affecting approximately 3 million people
It is generally believed that several risk factors are directly related to the pathogenesis of COPD, including host and environmental factors [3]
Relevant literatures reporting the relationship between polymorphisms of matrix metalloproteinase 9 (MMP9)-1562C/T and susceptibility to COPD in PubMed, Web of Science, VIP, Wanfang and CNKI databases were searched using the key words »matrix metalloproteinases 9/MMP9, COPD/chronic obstructive pulmonary disease«
Summary
Chronic obstructive pulmonary disease (COPD) is a worldwide disease affecting approximately 3 million people. It is estimated that COPD will be the third leading cause of death by 2020 [1]. As a chronic airway inflammatory disease, COPD is characterized by incomplete reversible airflow limitation, inflammatory cell infiltration, excessive mucus secretion, and airway remodeling [2]. The precise molecular mechanism underlying the pathogenesis of COPD remains unclear. It is generally believed that several risk factors are directly related to the pathogenesis of COPD, including host and environmental factors [3]. Among environmental factors, smoking, exposure to chemicals, indoor and outdoor air pollution are risk factors for COPD [4]. Host factors of COPD include antitrypsin-1, excessive deposition of extracellular matrix (ECM), corticosteroids, inflammatory stimuli, and metabolic imbalances [5, 6]
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