The emerging role of telomere biology in cardiovascular disease
The emerging role of telomere biology in cardiovascular disease
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DOI：
10.2741/3604
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发表时间：
2010-01-01
影响因子：
3.1
通讯作者：
van der Harst, Pim
中科院分区：
文献类型：
--
作者：
Huzen, Jardi;de Boer, Rudolf A.;van der Harst, Pim
心血管疾病的易感性、发病年龄和进展速度存在显著的差异。这是不充分的解释存在或不存在传统的风险因素。生物老化的差异可能是观察到的变异性的一个额外组成部分。端粒长度提供了一个潜在的个体的生物学年龄的标志，较短的端粒反映了更先进的生物学年龄。出生时端粒长度主要由遗传因素决定。端粒磨损是细胞复制的结果，并且可以被有害的环境因素如氧化应激加速。当端粒达到临界阈值时，细胞将进入衰老并变得功能失调。在患有衰老相关疾病的患者中，端粒明显较短，包括冠状动脉疾病和慢性心力衰竭。此外，许多传统的心血管危险因素与较短的端粒长度相关。如果能够证明端粒不仅与心血管疾病的发病机制相关，而且还与心血管疾病的发病机制有因果关系，那么它可能为未来预防和治疗策略的发展提供令人兴奋的新途径。
A striking variability exists in the susceptibility, age of onset and pace of progression of cardiovascular diseases. This is inadequately explained by the presence or absence of conventional risk factors. Differences in biological aging might provide an additional component of the observed variability. Telomere length provides a potential marker of an individual's biological age, shorter telomeres reflect a more advanced biological age. Telomere length at birth is mainly determined by genetic factors. Telomere attrition occurs as a consequence of cellular replication and can be accelerated by harmful environmental factors such as oxidative stress. When telomeres reach a critical threshold the cell will enter senescence and becomes dysfunctional. Telomeres are remarkably shorter in patients with aging associated diseases, including coronary artery disease and chronic heart failure. In addition, numerous conventional cardiovascular risk factors are associated with shorter telomere length. If telomeres can be proven to be not only associated but also causally involved in the pathogenesis of cardiovascular disease it might provide exciting new avenues for the development of future preventive and therapeutic strategies.