Ischemic acute kidney injury (AKI) is a frequent complication resulting from a myriad of conditions that decrease effective arterial blood volume to the kidneys including myocardial ischemia, sepsis, and hypovolemia. Following acute ischemic insult, restoration of renal blood flow inevitably leads to the aggravation of renal injury due to a widely researched condition known as ischemia/reperfusion (I/R) injury. For decades, apoptosis and necrosis have been proposed as being the two cell death pathways responsible for the pathogenesis of renal ischemic AKI. There is recent evidence to show that necrosis could be regulated in a caspase-independent manner. This regulated or programmed necrosis is termed necroptosis. Necroptotic markers such as receptor-interacting serine/threonine-protein kinase 1 (RIPK1), RIPK3, and mixed lineage kinase domain like pseudokinase (MLKL) have been identified in both in vitro and in vivo models of renal I/R injury, suggesting that necroptosis might be a potential therapeutic target to limit renal I/R injury. In this review, available reports from in vitro, in vivo and clinical reports regarding the association of necroptosis in renal I/R injury, along with its therapeutic potential, has been comprehensively summarized and discussed. Understanding this contributory mechanism could pave ways to improve therapeutic strategies in combating renal I/R injury.

缺血性急性肾损伤（AKI）是由多种情况引起的常见并发症，这些情况会降低肾脏的有效动脉血容量，包括心肌缺血，败血症和血容量不足。急性缺血性损伤后，由于被广泛研究的称为缺血/再灌注（I / R）损伤的状况，肾血流的恢复不可避免地导致肾损伤的加重。几十年来，已经提出凋亡和坏死是负责肾脏缺血性AKI发病机理的两种细胞死亡途径。最近的证据表明坏死可以以胱天蛋白酶独立的方式调节。这种调节的或程序性的坏死称为坏死性坏死。肾病标记物，例如与受体相互作用的丝氨酸/苏氨酸蛋白激酶1（RIPK1），RIPK3，肾I / R损伤的体外和体内模型，提示坏死性坏死可能是限制肾I / R损伤的潜在治疗靶点。在这篇综述中，关于肾脏I / R损伤中坏死病的相关性及其治疗潜力的体外，体内和临床报告的可利用报告已得到全面总结和讨论。了解这种贡献机制可能为改善抗肾I / R损伤的治疗策略铺平道路。