Wang Xinhui, Bonventre Joseph V, Parrish Alan R
Department of Medical Pharmacology and Physiology, School of Medicine, University of Missouri, Columbia, MO 65212, USA.
Renal Division and Biomedical Engineering Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Int J Mol Sci. 2014 Sep 1;15(9):15358-76. doi: 10.3390/ijms150915358.
Three decades have passed since a series of studies indicated that the aging kidney was characterized by increased susceptibility to nephrotoxic injury. Data from these experimental models is strengthened by clinical data demonstrating that the aging population has an increased incidence and severity of acute kidney injury (AKI). Since then a number of studies have focused on age-dependent alterations in pathways that predispose the kidney to acute insult. This review will focus on the mechanisms that are altered by aging in the kidney that may increase susceptibility to injury, including hemodynamics, oxidative stress, apoptosis, autophagy, inflammation and decreased repair.
一系列研究表明，衰老的肾脏对肾毒性损伤的易感性增加，自那时起已过去三十年。临床数据显示老年人群急性肾损伤（AKI）的发病率和严重程度有所增加，这进一步证实了这些实验模型的数据。从那时起，许多研究聚焦于使肾脏易受急性损伤的途径中与年龄相关的改变。本综述将关注肾脏衰老过程中发生改变的、可能增加损伤易感性的机制，包括血流动力学、氧化应激、细胞凋亡、自噬、炎症以及修复能力下降。
