Department of Cardiology, University Medical Centre Groningen, University of Groningen, Hanzeplein 1, 9700 RB Groningen, The Netherlands.
Front Biosci (Landmark Ed). 2010 Jan 1;15(1):35-45. doi: 10.2741/3604.
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.
心血管疾病的易感性、发病年龄和进展速度存在显著差异。这不能仅用传统危险因素的存在与否来解释。生物学衰老的差异可能为观察到的可变性提供额外的组成部分。端粒长度提供了个体生物学年龄的潜在标志物，较短的端粒反映了更先进的生物学年龄。出生时的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，并且可以被氧化应激等有害环境因素加速。当端粒达到临界阈值时，细胞将进入衰老并失去功能。与衰老相关的疾病（包括冠状动脉疾病和慢性心力衰竭）患者的端粒明显较短。此外，许多传统心血管危险因素与较短的端粒长度相关。如果可以证明端粒不仅与心血管疾病的发病机制相关，而且还与之相关，那么这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。
