{"title":"A Smoking-Associated miRNA-mRNA Coexpression Network.","authors":"Mete Civelek","doi":"10.1161/CIRCGENETICS.117.001914","DOIUrl":null,"url":null,"abstract":"Adverse effects of cigarette smoking on our health are well documented. On the other hand, we do not fully understand the mechanisms by which these adverse effects occur. In this issue of Circulation: Cardiovascular Genetics , Willinger et al1 identified a smoking-related microRNA (miRNA)/messenger RNA (mRNA) coexpressed gene network in the whole blood of previous and current smokers. They performed the study as part of the extensive phenotypic characterization performed in the participants of the Framingham Heart Study.2 miRNAs, which are small noncoding RNAs that regulate gene expression by binding to their target mRNAs causing translational repression or target degradation,3 have been recognized for their role in cardiovascular pathology.4–6 The results of the current study add another dimension to previous studies by pointing to dysregulated inflammatory responses in leukocytes by miRNA-specific gene regulatory networks in cigarette smokers.\n\nSee Article by Willinger and Rong et al \n\nThe authors arrived at this conclusion via a series of well-designed experiments. They used total RNA isolated from peripheral whole blood obtained from 5023 nonfasting participants of the Framingham Study. These participants were part of the Offspring and Third Generation cohorts. The mean age of the participants was 55 years old, and 54% of them were female. Ten percent of them were current smokers, 41% were former smokers, and 48% had …","PeriodicalId":10277,"journal":{"name":"Circulation: Cardiovascular Genetics","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2017-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1161/CIRCGENETICS.117.001914","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Circulation: Cardiovascular Genetics","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1161/CIRCGENETICS.117.001914","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 1
Abstract
Adverse effects of cigarette smoking on our health are well documented. On the other hand, we do not fully understand the mechanisms by which these adverse effects occur. In this issue of Circulation: Cardiovascular Genetics , Willinger et al1 identified a smoking-related microRNA (miRNA)/messenger RNA (mRNA) coexpressed gene network in the whole blood of previous and current smokers. They performed the study as part of the extensive phenotypic characterization performed in the participants of the Framingham Heart Study.2 miRNAs, which are small noncoding RNAs that regulate gene expression by binding to their target mRNAs causing translational repression or target degradation,3 have been recognized for their role in cardiovascular pathology.4–6 The results of the current study add another dimension to previous studies by pointing to dysregulated inflammatory responses in leukocytes by miRNA-specific gene regulatory networks in cigarette smokers.
See Article by Willinger and Rong et al
The authors arrived at this conclusion via a series of well-designed experiments. They used total RNA isolated from peripheral whole blood obtained from 5023 nonfasting participants of the Framingham Study. These participants were part of the Offspring and Third Generation cohorts. The mean age of the participants was 55 years old, and 54% of them were female. Ten percent of them were current smokers, 41% were former smokers, and 48% had …
期刊介绍:
Circulation: Genomic and Precision Medicine considers all types of original research articles, including studies conducted in human subjects, laboratory animals, in vitro, and in silico. Articles may include investigations of: clinical genetics as applied to the diagnosis and management of monogenic or oligogenic cardiovascular disorders; the molecular basis of complex cardiovascular disorders, including genome-wide association studies, exome and genome sequencing-based association studies, coding variant association studies, genetic linkage studies, epigenomics, transcriptomics, proteomics, metabolomics, and metagenomics; integration of electronic health record data or patient-generated data with any of the aforementioned approaches, including phenome-wide association studies, or with environmental or lifestyle factors; pharmacogenomics; regulation of gene expression; gene therapy and therapeutic genomic editing; systems biology approaches to the diagnosis and management of cardiovascular disorders; novel methods to perform any of the aforementioned studies; and novel applications of precision medicine. Above all, we seek studies with relevance to human cardiovascular biology and disease.