Tsirpanlis George
Department of Nephrology, General Hospital of Athens, Athens, Greece.
Am J Kidney Dis. 2008 Jan;51(1):131-44. doi: 10.1053/j.ajkd.2007.07.035.
Cellular senescence is associated with shortened or damaged telomeres and is characterized by permanent exit from the cell cycle, morphological changes, and altered function. It develops after repeated cell divisions and also can be induced prematurely by stress conditions. The senescent phenotype, depending on cell type and atherosclerosis phase, seems to be a proatherosclerotic one: it promotes endothelial dysfunction and appears to be implicated in plaque destabilization, as well as in endothelial progenitor cell alteration. Many traditional and nontraditional cardiovascular disease risk factors induce senescence in a variety of vascular cells. Several of these factors, such as diabetes, hypertension, oxidative stress, and inflammation, are clustered in patients with chronic kidney disease. In a limited number of recent studies, stress-induced premature cellular senescence in this biologically aged population also was described. The hypothesis that premature cellular senescence might be considered an additional atherosclerosis-inducing factor in patients with chronic kidney disease is proposed.
细胞衰老与端粒缩短或受损有关，其特征是永久性退出细胞周期、形态变化和功能改变。它在细胞反复分裂后出现，也可由应激条件过早诱导。衰老表型取决于细胞类型和动脉粥样硬化阶段，似乎是促动脉粥样硬化的：它促进内皮功能障碍，似乎与斑块不稳定以及内皮祖细胞改变有关。许多传统和非传统的心血管疾病危险因素可在多种血管细胞中诱导衰老。其中一些因素，如糖尿病、高血压、氧化应激和炎症，在慢性肾病患者中聚集。在最近的一些有限研究中，也描述了在这个生物学上衰老的人群中应激诱导的过早细胞衰老。有人提出这样的假说，即过早细胞衰老可能被认为是慢性肾病患者动脉粥样硬化的一个额外诱导因素。
