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Gene-air pollution interaction and cardiovascular disease: a review
Authors:Zanobetti Antonella  Baccarelli Andrea  Schwartz Joel
Affiliation:
  • Department of Environmental Health, Exposure Epidemiology and Risk Program, Harvard School of Public Health, Boston, MA 02115
  • Abstract:Genetic susceptibility is likely to play a role in response to air pollution. Hence, gene-environment interaction studies can be a tool for exploring the mechanisms and the importance of the pathway in the association between air pollution and a cardiovascular outcome.In this article, we present a systematic review of the studies that have examined gene-environment interactions in relation to the cardiovascular health effects of air pollutants.We identified 16 articles meeting our search criteria. Of these studies, most have focused on individual functional polymorphisms or individual candidate genes. Moreover, they were all based on 3 study populations that have been extensively investigated in relation to air pollution effects: the Normative Aging Study, Air Pollution and Inflammatory Response in Myocardial Infarction Survivors: Gene-Environment Interaction in a High Risk Group, and Multiethnic Study of Atherosclerosis.In conclusions, the studies differed substantially in both the cardiovascular outcomes examined and the polymorphisms examined, so there is little confirmation of results across cohorts. Gene-environment interaction studies can help explore the mechanisms and the potential pathway in the association between air pollution and a cardiovascular outcome; replication of findings and studies involving multiple cohorts would be needed to draw stronger conclusions.
    Keywords:ACE, angiotensin-I converting enzyme   ADRB2, β2-adrenergic receptor   AGT, angiotensinogen   AGTR1, type 1 angiotensin II receptor   ALOX15, arachidonate 15-lipoxygenase   APOE, apolipoprotein E   BC, black carbon   BP, blood pressure   CRP, C-reactive protein   cSHMT, cytoplasmic serine hydroxymethyltransferase   CVD, cardiovascular disease   DGCR8, DiGeorge critical region-8   EDN1, endothelin 1   GRK4, G protein-coupled receptor kinase 4   GSS, genetic susceptibility score   GSTM1, glutathione S-transferase μ1   GSTP1, glutathione S-transferase π1   GSTT1, glutathione S-transferase θ1   GT, guanine thymine   GWAS, genome-wide association study   HFE, hemocromatosis   HMOX-1, heme oxygenase 1   HRV, heart rate variability   IL-6, interleukin 6   ITPR2, inositol 1,4,5-triphosphate receptor 2   LPL, lipoprotein lipase   LVM, left ventricular mass   MESA, Multiethnic Study of Atherosclerosis   MI, myocardial infarction   miRNA, microRNA   MTHFR, methylenetetrahydrofolate reductase   NAS, Normative Aging Study   NQO1, NAD(P)H dehydrogenase, quinone 1   PM, particulate matter   PTGS1, prostaglandin-endoperoxide synthase 1   PTGS2, prostaglandin-endoperoxide synthase 2   ROS, reactive oxygen species   SNP, single-nucleotide polymorphism   TLR4, toll-like receptor 4   VEGF, vascular endothelial growth factor
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