Department of Pharmacology and Toxicology, Nijmegen Centre for Molecular Life Sciences, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.
Apoptosis. 2009 Dec;14(12):1451-8. doi: 10.1007/s10495-009-0359-1.
Increased levels of reactive oxygen species (ROS) by hyperglycemia can induce apoptosis of renal cells and diabetic nephropathy. The redox balance in the renal cell seems, therefore, of the utmost importance. ROS-mediated apoptosis may be further aggravated by an inadequate cytoprotective response against ROS. When there are insufficient cytoprotective and ROS scavenging molecules, ROS lead to considerable cellular damage and to a point of no return in apoptosis. Induction of cytoprotective proteins may prevent or attenuate apoptosis, renal cell injury, and finally diabetic nephropathy. Here, we discuss some mechanisms of apoptosis and several strategies that have been probed to ameliorate, or to prevent apoptosis in the diabetic kidney.
高血糖引起的活性氧（ROS）水平升高可诱导肾细胞凋亡和糖尿病肾病。因此，肾细胞中的氧化还原平衡似乎至关重要。ROS 介导的细胞凋亡可能会因对 ROS 的细胞保护反应不足而进一步加重。当细胞保护和 ROS 清除分子不足时，ROS 会导致相当大的细胞损伤，并使细胞凋亡达到不可逆转的程度。诱导细胞保护蛋白可能预防或减轻细胞凋亡、肾细胞损伤，并最终预防糖尿病肾病。在这里，我们讨论了几种细胞凋亡的机制，并探讨了一些改善或预防糖尿病肾脏中细胞凋亡的策略。
