Price Peter M, Megyesi Judit, Safirstein Robert L
Department of Internal Medicine, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.
Semin Nephrol. 2003 Sep;23(5):449-59. doi: 10.1016/s0270-9295(03)00087-1.
Research into mechanisms of acute renal failure has begun to reveal molecular targets for possible therapeutic intervention. Much useful knowledge into the causes and prevention of this syndrome has been gained by the study of animal models. Most recently, investigation of the effects on acute renal failure of selected gene knock-outs in mice has contributed to our recognition of many previously unappreciated molecular pathways. Particularly, experiments have revealed the protective nature of 2 highly induced genes whose functions are to inhibit and control the cell cycle after acute renal failure. By use of these models we have started to understand the role of increased cell cycle activity after renal stress and the role of proteins induced by these stresses that limit this proliferation.
对急性肾衰竭机制的研究已开始揭示可能进行治疗干预的分子靶点。通过对动物模型的研究，我们已获得了许多关于该综合征病因及预防的有用知识。最近，对小鼠特定基因敲除对急性肾衰竭影响的研究，有助于我们认识许多以前未被重视的分子途径。特别是，实验揭示了2种高度诱导基因的保护性质，其功能是在急性肾衰竭后抑制和控制细胞周期。通过使用这些模型，我们已开始了解肾应激后细胞周期活性增加的作用，以及这些应激诱导的限制细胞增殖的蛋白质的作用。
