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Notable epigenetic role of hyperhomocysteinemia in atherogenesis

机译:高同型半胱氨酸血症在动脉粥样硬化中的显着表观遗传学作用

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摘要

Atherosclerosis is associated with multiple genetic and modifiable risk factors. There is an increasing body of evidences to indicate that epigenetic mechanisms also play an essential role in atherogenesis by influencing gene expression. Homocysteine is a sulfur-containing amino acid formed during methionine metabolism. Elevated plasma level of homocysteine is generally termed as hyperhomocysteinemia. As a potential risk factor for cardiovascular diseases, hyperhomocysteinemia may initiate or motivate atherogenesis by modification of DNA methylation. The underlying epigenetic mechanism is still unclear with controversial findings. This review focuses on epigenetic involvement and mechanisms of hyperhomocysteinemia in atherogenesis. Considering the potential beneficial effects of anti-homocysteinemia treatments in preventing atherosclerosis, further studies on the role of hyperhomocysteinemia in atherogenesis are warranted.
机译:动脉粥样硬化与多种遗传和可改变的危险因素有关。越来越多的证据表明表观遗传机制通过影响基因表达在动脉粥样硬化中也起着重要作用。同型半胱氨酸是蛋氨酸代谢过程中形成的含硫氨基酸。高半胱氨酸的血浆水平升高通常被称为高同型半胱氨酸血症。高半胱氨酸血症作为心血管疾病的潜在危险因素,可能通过修饰DNA甲基化而引发或激发动脉粥样硬化。尚有争议的结果尚不清楚潜在的表观遗传机制。这篇综述着重于表观遗传参与和高同型半胱氨酸在动脉粥样硬化中的机制。考虑到抗高半胱氨酸血症治疗在预防动脉粥样硬化中的潜在有益作用,有必要对高半胱氨酸血症在动脉粥样硬化中的作用进行进一步研究。

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