Zhao Yuqi, Blencowe Montgomery, Shi Xingyi, Shu Le, Levian Candace, Ahn In Sook, Kim Stuart K, Huan Tianxiao, Levy Daniel, Yang Xia
Department of Integrative Biology and Physiology, University of California, Los Angeles, Los Angeles, CA, United States.
Department of Genetics, Department of Developmental Biology, Stanford University Medical Center, Stanford, CA, United States.
Front Cardiovasc Med. 2019 Mar 12;6:21. doi: 10.3389/fcvm.2019.00021. eCollection 2019.
Blood pressure (BP) is a highly heritable trait and a major cardiovascular disease risk factor. Genome wide association studies (GWAS) have implicated a number of susceptibility loci for systolic (SBP) and diastolic (DBP) blood pressure. However, a large portion of the heritability cannot be explained by the top GWAS loci and a comprehensive understanding of the underlying molecular mechanisms is still lacking. Here, we utilized an integrative genomics approach that leveraged multiple genetic and genomic datasets including (a) GWAS for SBP and DBP from the International Consortium for Blood Pressure (ICBP), (b) expression quantitative trait loci (eQTLs) from genetics of gene expression studies of human tissues related to BP, (c) knowledge-driven biological pathways, and (d) data-driven tissue-specific regulatory gene networks. Integration of these multidimensional datasets revealed tens of pathways and gene subnetworks in vascular tissues, liver, adipose, blood, and brain functionally associated with DBP and SBP. Diverse processes such as platelet production, insulin secretion/signaling, protein catabolism, cell adhesion and junction, immune and inflammation, and cardiac/smooth muscle contraction, were shared between DBP and SBP. Furthermore, "Wnt signaling" and "mammalian target of rapamycin (mTOR) signaling" pathways were found to be unique to SBP, while "cytokine network", and "tryptophan catabolism" to DBP. Incorporation of gene regulatory networks in our analysis informed on key regulator genes that orchestrate tissue-specific subnetworks of genes whose variants together explain ~20% of BP heritability. Our results shed light on the complex mechanisms underlying BP regulation and highlight potential novel targets and pathways for hypertension and cardiovascular diseases.
血压(BP)是一种高度可遗传的性状,也是主要的心血管疾病风险因素。全基因组关联研究(GWAS)已发现了许多与收缩压(SBP)和舒张压(DBP)相关的易感基因座。然而,很大一部分遗传力无法由顶级GWAS基因座解释,对潜在分子机制仍缺乏全面了解。在此,我们采用了一种整合基因组学方法,该方法利用了多个遗传和基因组数据集,包括:(a)来自国际血压联盟(ICBP)的SBP和DBP的GWAS;(b)来自与血压相关的人体组织基因表达研究的表达定量性状基因座(eQTL);(c)知识驱动的生物途径;以及(d)数据驱动的组织特异性调控基因网络。整合这些多维数据集揭示了血管组织、肝脏、脂肪、血液和大脑中数十条与DBP和SBP功能相关的途径和基因子网。血小板生成、胰岛素分泌/信号传导、蛋白质分解代谢、细胞粘附和连接、免疫和炎症以及心脏/平滑肌收缩等多种过程在DBP和SBP之间是共有的。此外,发现“Wnt信号传导”和“雷帕霉素哺乳动物靶标(mTOR)信号传导”途径是SBP特有的,而“细胞因子网络”和“色氨酸分解代谢”是DBP特有的。在我们的分析中纳入基因调控网络,确定了关键调控基因,这些基因协调组织特异性基因子网,其变体共同解释了约20%的血压遗传力。我们的结果揭示了血压调节的复杂机制,并突出了高血压和心血管疾病潜在的新靶点和途径。