细胞铁死亡在急性肾功能损伤中的研究进展

Research progress of ferroptosis in acute renal injury

急性肾损伤是由各种病理、药物等因素引起的短时间内肾功能突然或持续下降。近年来,铁死亡作为一种新的调控性细胞死亡方式被逐渐认识,其由细胞谷胱甘肽抗氧化防御系统的失活,导致脂质过氧化产物和活性氧堆积诱发。铁死亡代谢网络和体内分子信号网络以及多种病理反应途径存在交互作用,并被认为与急性肾损伤的病理生理过程密切相关,抑制肾小管上皮细胞铁死亡可有效缓解急性肾损伤的发生发展,目前围绕靶向铁死亡的急性肾损伤治疗策略在肾脏疾病研究中已成为一大研究热点。该文主要就铁死亡的发生调控机制、与急性肾损伤的关系以及靶向铁死亡的治疗策略进行综述,以期为急性肾损伤的治疗提供新的视角。

Acute kidney injury is defined as a rapid or continuous decline in renal function caused by a variety of pathological,drug,and other factors.In recent years,ferroptosis has been gradually recognized as a new regulatory cell death mode,which is induced by the inactivation of the cellular glutathione antioxidant defense system,leading to the accumulation of lipid peroxidation products and reactive oxygen species.The metabolic network of ferroptosis interacts with the molecular signaling network and various pathologic response pathways,which is thought to be closely related to the pathophysiological process of acute kidney injury.Inhibiting ferroptosis in renal tubular epithelial cells can effectively alleviate the occurrence and development of acute kidney injury.Currently,targeting ferroptosis on acute kidney injury treatment strategies has become a hotspot in kidney disease.This review summarizes the regulatory mechanism and the relationship of ferroptosis with acute kidney injury,as well as the therapeutic strategies targeting ferroptosis,to provide new perspective for the treatment of acute kidney injury.