复制性衰老与心血管健康之间存在一定的关系。

Maria E Karavassilis, Richard Faragher
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引用次数: 7

摘要

越来越多的证据表明,衰老细胞的积累是一种看似合理的衰老机制。有人提出,血管细胞的衰老在心血管疾病的发展中起着因果作用。从这一假设中得出的一个关键预测是,与来自无疾病对照的细胞相比,来自心血管疾病供体的细胞培养物的体外复制能力会降低。因此,我们对供体年龄、心血管健康状况和体外培养血管平滑肌和内皮细胞获得的最大群体倍增水平之间的关系进行了正式审查。我们获得了202个独立细胞培养的数据。内皮细胞和血管平滑肌细胞的复制能力与供体年龄呈反比关系。与年龄匹配的健康对照相比,来自心血管疾病供体的培养物显示出较低的总体复制潜力。一般来说,研究发现,在生命之初,那些没有患病的个体的繁殖潜力高于那些患病的个体,两组中年龄匹配的个体的平均累积种群加倍(CPDs)的差异在整个生命周期中大致保持不变。这些结果与模型一致,即血管细胞的遗传复制能力是晚年心血管疾病发病的一个更强的决定因素,而不是整个生命过程中的磨损。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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A relationship exists between replicative senescence and cardiovascular health.

A growing body of evidence demonstrates that the accumulation of senescent cells is a plausible ageing mechanism. It has been proposed that the senescence of vascular cells plays a causal role in the development of cardiovascular pathologies. A key prediction arising from this hypothesis is that cultures of cells derived from donors with cardiovascular disease will show reduced in vitro replicative capacities compared to those derived from disease-free controls. Accordingly, we carried out a formal review of the relationship among donor age, cardiovascular health status and maximum population doubling level attained in vitro by cultures of vascular smooth muscle and endothelial cells. Data were available to us on a total of 202 independent cell cultures. An inverse relationship was found to exist between replicative capacity and donor age in both endothelial and vascular smooth muscle cells. Cultures derived from donors with cardiovascular disease showed a lower overall replicative potential than age-matched healthy controls. In general the replicative potential at the start of the lifespan was found to be higher in those individuals without disease than those with disease and the difference in average cumulative population doublings (CPDs) in age-matched individuals in the two groups remained roughly constant throughout the lifetime. These results are consistent with the model in which the inherited replicative capacity of vascular cells is a stronger determinant of the onset of cardiovascular disease later in life, than wear-and-tear throughout the life course.

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