Stress-induced premature senescence of endothelial cells: a perilous state between recovery and point of no return
Stress-induced premature senescence of endothelial cells: a perilous state between recovery and point of no return
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DOI：
10.1097/moh.0b013e32832a07bd
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发表时间：
2009-05-01
影响因子：
3.2
通讯作者：
Patschan, Susann
中科院分区：
文献类型：
--
作者：
Goligorsky, Michael S.;Chen, Jun;Patschan, Susann
综述目的：综述近年来有关应激诱导血管内皮细胞早衰（SIPS）的形态学和分子机制的研究，并对晚期糖基化终产物（AGEs）诱导SIPS的溶酶体功能障碍和自噬受损进行了阐述。最近，在预防和逆转衰老方面取得了进展。溶酶体功能障碍和Lamp-2A缺陷在衰老中的作用已经得到证实。分子分析确定了sirtuin 1在防止细胞衰老中的作用;阐明了polycomb group（PcG）蛋白Bmi-1在衰老中的作用。此外，关于小窝蛋白-1在细胞衰老中的作用的有趣的数据已经出现。SummaryIn衰老的生物体和慢性疾病正常运作的组织被衰老的细胞所取代。复制性衰老和SIPS之间的比较表明，复制性衰老几乎完全与端粒酶活性的降低和端粒的磨损，而SIPS不需要这些事件，从而赋予这个过程的潜在可逆性。
Purpose of reviewTo discuss most recently published studies on morphologic patterns and molecular mechanisms of stress-induced premature senescence (SIPS) of vascular endothelial cells.Recent findingsLysosomal dysfunction and impaired autophagy, which have been well established in replicative senescence, were also described in SIPS induced by advanced glycation end products (AGEs). Recently, strides were made to prevent and reverse senescence. The role of lysosomal dysfunction and Lamp-2A deficiency has been demonstrated in aging. Molecular analyses identified the role of sirtuin 1 in preventing cell senescence; shed light on the role of polycomb group (PcG) protein Bmi-1 in senescence. Additionally, intriguing data on the role of caveolin-1 in cell senescence have emerged.SummaryIn aging organisms and chronic diseases properly functioning tissue is replaced by senescent cells. Comparison between replicative senescence and SIPS indicates that replicative senescence is almost exclusively associated with the reduction of telomerase activity and attrition of telomeres, whereas SIPS does not require these events, thus conferring potential reversibility onto this process.