首页> 外文期刊>Circulation: An Official Journal of the American Heart Association >Epigenetic control of angiogenesis via DNA methylation.
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Epigenetic control of angiogenesis via DNA methylation.

机译:通过DNA甲基化对血管生成进行表观遗传控制。

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Why some patients develop limb- and life-saving collaterals but others do not constitutes one of the great challenges that face patients with peripheral vascular and coronary artery disease. A longstanding goal in vascular disease is the establishment of therapies that enhance angio-genesis in compromised tissue beds. To achieve this goal, however, it is essential to define and understand the underlying mechanisms that control angiogenesis and may distinguish individual patient capacity for collateral formation. In this issue of Circulation, Rao and colleagues report that ischemic injury increases DNA methylation in several genes critical for angiogenesis. The methyl-CpG-binding domain 2 (MBD2) protein senses DNA methylation and mediates transcriptional repression of genes involved in angiogenesis and endothelial cell survival. This seminal report mechanistically links epigenetic changes in vascular cells to angiogenesis, paving the way for new therapies that could improve perfusion in patients with vascular disease.
机译:为什么有些患者发展出能挽救肢体和挽救生命的侧支,而另一些却没有成为周围血管和冠状动脉疾病患者面临的巨大挑战之一。血管疾病的长期目标是建立能够增强受损组织床中血管生成的疗法。但是,要实现此目标,必须定义和理解控制血管生成并可能区分患者个体侧支形成能力的潜在机制。在《循环》杂志上,Rao及其同事报道了缺血性损伤会增加一些对血管生成至关重要的基因的DNA甲基化。甲基CpG结合域2(MBD2)蛋白可感知DNA甲基化并介导与血管生成和内皮细胞存活有关的基因的转录抑制。这项开创性的报告将血管细胞的表观遗传学变化与血管生成机械性地联系在一起,为可以改善血管疾病患者灌注的新疗法铺平了道路。

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