Supplementary Material for: Molecular Mechanisms of Renal Ischemic Conditioning Strategies

Ischemia-reperfusion injury is the leading cause of acute kidney injury in a variety of clinical settings such as renal transplantation and hypovolemic and/or septic shock. Strategies to reduce ischemia-reperfusion injury are obviously clinically relevant. Ischemic conditioning is an inherent part of the renal defense mechanism against ischemia and can be triggered by short periods of intermittent ischemia and reperfusion. Understanding the signaling transduction pathways of renal ischemic conditioning can promote further clinical translation and pharmacological advancements in this era. This review summarizes research on the molecular mechanisms underlying both local and remote ischemic pre-, per- and postconditioning of the kidney. The different types of conditioning strategies in the kidney recruit similar powerful pro-survival mechanisms. Likewise, renal ischemic conditioning mobilizes many of the same protective signaling pathways as in other organs, but differences are recognized.

缺血再灌注损伤（ischemia-reperfusion injury）是肾移植、低血容量性休克及感染性休克等多种临床场景中急性肾损伤的最主要诱因。降低缺血再灌注损伤的相关策略显然具有重要临床价值。缺血适应（ischemic conditioning）是肾脏对抗缺血的固有防御机制的组成部分，可通过短暂的间歇性缺血与再灌注过程触发。阐明肾脏缺血适应的信号转导通路，能够推动该领域在当前时代的进一步临床转化与药学研究进展。本综述总结了针对肾脏局部与远程缺血预处理、缺血中处理及缺血后处理的分子机制相关研究。肾脏的各类缺血适应策略均能激活相似的强效促存活信号通路。同样，肾脏缺血适应所动员的保护性信号通路与其他器官中的同类通路高度相似，但二者之间也存在已被证实的差异。