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[心血管疾病中的端粒与生物衰老]

[Telomeres and biological ageing in cardiovascular disease].

作者信息

Huzen J, van Veldhuisen D J, van Gilst W H, van der Harst P

机构信息

Universitair Medisch Centrum Groningen, afd. Cardiologie, Postbus 30.001, 9700 RB Groningen.

出版信息

Ned Tijdschr Geneeskd. 2008 May 31;152(22):1265-70.

Abstract

The striking variability in the age of onset of and the manifestation/ absence of manifestation of cardiovascular diseases is inadequately explained by conventional risk factors, but may be explained by variation in biological age. Telomere length is possibly a reliable marker of biological age, shorter telomeres reflecting more advanced age. The initial telomere length ofa person is mainly determined by genetic factors. Moreover, the telomere length shortens with each cell division, and exposition to harmful environmental factors also results in shorter telomeres. Leukocytes of patients with atherosclerosis and heart failure display remarkably shorter telomeres compared to leukocytes of healthy subjects of similar age. Conventional cardiovascular risk factors are also associated with telomere length. If telomeres are indeed causally involved in the pathogenesis of cardiovascular disease, this might provide new avenues for future preventive and therapeutic strategies.

摘要

心血管疾病发病年龄以及是否出现症状的显著变异性,传统风险因素对此解释并不充分,但可能由生物学年龄的差异来解释。端粒长度可能是生物学年龄的可靠标志物,较短的端粒反映年龄更大。一个人的初始端粒长度主要由遗传因素决定。此外,端粒长度随每次细胞分裂而缩短,暴露于有害环境因素也会导致端粒变短。与年龄相仿的健康受试者的白细胞相比,动脉粥样硬化和心力衰竭患者的白细胞端粒明显更短。传统心血管风险因素也与端粒长度有关。如果端粒确实在心血管疾病发病机制中起因果作用,这可能为未来的预防和治疗策略提供新途径。

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