Epigenomes: the missing heritability in human cardiovascular disease?
Epigenomes: the missing heritability in human cardiovascular disease?
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DOI：
10.1002/prca.201400031
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发表时间：
2014-08
影响因子：
2
通讯作者：
Vondriska, Thomas M.
中科院分区：
文献类型：
--
作者：
Monte, Emma;Vondriska, Thomas M.
心血管疾病是人类健康的巨大负担，是各种生物分子网络在环境应激背景下发生故障的结果。尽管有强有力的证据表明可遗传性，但许多常见形式的心脏病(特别是心力衰竭)并未屈服于全基因组关联研究，以确定通过单个分子的破坏而起作用的致病突变。然而，越来越多的证据表明，非编码区的遗传变异与疾病易感性密切相关。我们假设，在没有蛋白质或mRNA序列和丰度变化的情况下，表观基因组变异可能会产生不同的染色质环境。通过这种方式，不同的遗传编码的染色质环境可以对导致心力衰竭的环境压力表现出不同的反应，这解释了在人类疾病中观察到的易感性改变的很大一部分原因。
Cardiovascular disease is a tremendous burden on human health and results from malfunction of various networks of biological molecules in the context of environmental stress. Despite strong evidence of heritability, many common forms of heart disease (heart failure in particular) have not yielded to genome-wide association studies to identify causative mutations acting via the disruption of individual molecules. Increasing evidence suggests, however, that genetic variation in non-coding regions is strongly linked to disease susceptibility. We hypothesize that epigenomic variation may engender different chromatin environments in the absence of (or in parallel with) changes in protein or mRNA sequence and abundance. In this manner, distinct—genetically encoded—chromatin environments can exhibit distinct responses to environmental stresses that cause heart failure, explaining a significant portion of the altered susceptibility that is observed in human disease.
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影响因子：
4.5
作者：
Farber CR;Bennett BJ;Orozco L;Zou W;Lira A;Kostem E;Kang HM;Furlotte N;Berberyan A;Ghazalpour A;Suwanwela J;Drake TA;Eskin E;Wang QT;Teitelbaum SL;Lusis AJ
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通讯作者：
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通讯作者：
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