Aging, Cellular Senescence, and Kidney Fibrosis
Aging, Cellular Senescence, and Kidney Fibrosis
复制标题
DOI：
10.1007/s40139-017-0143-9
复制
发表时间：
2017-06-01
影响因子：
--
通讯作者：
Schmitt, Roland
中科院分区：
文献类型：
--
作者：
Susnik, Nathan;Sen, Payel;Schmitt, Roland
纤维化是慢性肾脏病的一个标志，而慢性肾脏病的主要危险因素是年龄。衰老细胞在自然衰老期间和损伤后在肾脏中积累。了解衰老对肾脏维护的影响以及衰老与纤维化的关系可能会揭示新的治疗机会。最近的发现肾脏中衰老细胞的负荷可预测生物学年龄，并与肾脏疾病和同种异体移植物结局相关。衰老细胞不增殖以修复损伤。相反，它们分泌蛋白质，增强炎症和调节纤维化。药物阻断这些影响或消除衰老细胞可以抵消与年龄相关的diseases.Summary这篇综述探讨了衰老，细胞衰老，炎症和肾纤维化之间的关系。从不同学科的数据中，我们讨论了衰老相关的分泌表型，klotho和senotherapy，分析研究并寻找与年龄相关的肾纤维化的新解决方案。
Purpose of Review Fibrosis is a hallmark of chronic kidney disease, and a primary risk factor for chronic kidney disease is age. Senescent cells accumulate in the kidney during natural aging and after injury. Understanding the effect of senescence on kidney maintenance and how senescence is linked to fibrosis may reveal new therapeutic opportunities.Recent Findings The load of senescent cells in the kidney is predictive of biological age and correlates with renal disease and allograft outcome. Senescent cells do not proliferate to repair injury. Instead, they secrete proteins that enhance inflammation and modulate fibrosis. Pharmaceutical blockade of these effects or elimination of senescent cells can counteract age-related disease.Summary This review explores the relationships among aging, cellular senescence, inflammation, and kidney fibrosis. Drawing from data from various disciplines, we discuss senescence-associated secretory phenotype, klotho, and senotherapy, analyzing the research and looking for new solutions to age-related kidney fibrosis.