Kidney Int. 2012 Jun;81(12):1161-4. doi: 10.1038/ki.2012.36.
Acute kidney injury triggers activation of innate immune responses and of proapoptotic programs such as the p53 pathway. Mulay et al. examine the effects of blocking murine double minute-2 (mdm2), a negative regulator of p53, using a novel chemotherapeutic agent, nutlin-3a, in mouse ischemia-reperfusion injury. Their results indicate that mdm2 promotes renal regeneration by limiting p53-mediated apoptosis but also enhances early inflammation by facilitating DNA binding of nuclear factor-κB independently of p53.
急性肾损伤会引发固有免疫反应和促凋亡程序（如 p53 途径）的激活。Mulay 等人研究了使用新型化疗药物 nutlin-3a 阻断 p53 的负调节剂鼠双微体 2 (mdm2)对小鼠缺血再灌注损伤的影响。他们的结果表明，mdm2 通过限制 p53 介导的细胞凋亡促进肾脏再生，但也通过促进核因子-κB 的 DNA 结合来增强早期炎症，而与 p53 无关。
