Edo María Dolores, Andrés Vicente
Laboratory of Vascular Biology, Department of Molecular and Cellular Pathology and Therapy, Instituto de Biomedicina de Valencia, C/Jaime Roig 11, 46010, Valencia, Spain.
Cardiovasc Res. 2005 May 1;66(2):213-21. doi: 10.1016/j.cardiores.2004.09.007.
Although the level and pace of population aging display high geographical variability, virtually all countries have been experiencing growth in their elderly population, particularly in developed nations. Because aging is a major risk factor for atherosclerosis and associated disease, it is of up most importance to unravel the molecular mechanisms involved in vascular aging. Telomeres are specialized DNA-protein structures located at the ends of eukaryotic chromosomes whose length is progressively reduced in most somatic cells during aging. It is accepted that telomere exhaustion contributes to organismal ageing at least by impairing cell proliferation and viability. An emerging question is whether telomere erosion contributes to atherosclerosis. Here we discuss recent advances on the molecular control of telomere length in vascular cells, as well as animal and human studies that address the role of telomeres in vascular pathobiology. Although the interrelationships between telomere length and cardiovascular disease appear obvious, a chief question that remains unanswered is whether telomere ablation is cause of vascular injury or a surrogate phenomenon.
尽管人口老龄化的程度和速度呈现出高度的地域差异，但几乎所有国家的老年人口都在增长，尤其是在发达国家。由于衰老 是动脉粥样硬化及相关疾病的主要风险因素，因此阐明血管衰老所涉及的分子机制至关重要。端粒是位于真核染色体末端的特殊DNA-蛋白质结构，在衰老过程中，大多数体细胞中的端粒长度会逐渐缩短。人们认为，端粒损耗至少通过损害细胞增殖和活力而导致机体衰老。一个新出现的问题是，端粒缩短是否会导致动脉粥样硬化。在此，我们讨论血管细胞中端粒长度分子调控方面的最新进展，以及探讨端粒在血管病理生物学中作用的动物和人体研究。尽管端粒长度与心血管疾病之间的相互关系似乎很明显，但一个尚未得到解答的主要问题是，端粒缺失是血管损伤的原因还是一种替代现象。
