Han Zhongyu, Luo Yuanke, Chen Haoran, Zhang Guochen, You Luling, Zhang Meiqi, Lin Yumeng, Yuan Lan, Zhou Shiyi
School of Medical and Life Sciences, Chengdu University of Traditional Chinese Medicine, Chengdu, China.
School of Basic Medical Sciences, Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Kidney Dis (Basel). 2024 Mar 8;10(3):224-236. doi: 10.1159/000538106. eCollection 2024 Jun.
Ferroptosis, a newly recognized form of programmed cell death, is distinguished by its reliance on reactive oxygen species and iron-mediated lipid peroxidation, setting it apart from established types like apoptosis, cell necrosis, and autophagy. Recent studies suggest its role in exacerbating or mitigating diseases by influencing metabolic and signaling pathways in conditions such as tumors and ischemic organ damage. Evidence also links ferroptosis to various kidney diseases, prompting a review of its research status and potential breakthroughs in understanding and treating these conditions.
In acute kidney disease (AKI), ferroptosis has been confirmed in animal kidneys after being induced by various factors such as renal ischemia-reperfusion and cisplatin, and glutathione peroxidase 4 (GPX4) is linked with AKI. Ferroptosis is associated with renal fibrosis in chronic kidney disease (CKD), TGF-β1 being crucial in this regard. In diabetic nephropathy (DN), high SLC7A11 and low nuclear receptor coactivator 4 (NCOA4) expressions are linked to disease progression. For polycystic kidney disease (PKD), ferroptosis promotes the disease by regulating ferroptosis in kidney tissue. Renal cell carcinoma (RCC) and lupus nephritis (LN) also have links to ferroptosis, with mtDNA and iron accumulation causing RCC and oxidative stress causing LN.
Ferroptosis is a newly identified form of programmed cell death that is associated with various diseases. It targets metabolic and signaling pathways and has been linked to kidney diseases such as AKI, CKD, PKD, DN, LN, and clear cell RCC. Understanding its role in these diseases could lead to breakthroughs in their pathogenesis, etiology, and treatment.
铁死亡是一种新发现的程序性细胞死亡形式，其特点是依赖活性氧和铁介导的脂质过氧化，这使其有别于凋亡、细胞坏死和自噬等已确定的细胞死亡类型。最近的研究表明，它通过影响肿瘤和缺血性器官损伤等疾病状态下的代谢和信号通路，在疾病的加重或缓解中发挥作用。有证据还将铁死亡与各种肾脏疾病联系起来，促使人们对其研究现状以及在理解和治疗这些疾病方面的潜在突破进行综述。
在急性肾损伤（AKI）中，肾缺血再灌注和顺铂等多种因素诱导后，动物肾脏中已证实存在铁死亡，且谷胱甘肽过氧化物酶4（GPX4）与AKI有关。铁死亡与慢性肾脏病（CKD）中的肾纤维化相关，转化生长因子-β1（TGF-β1）在这方面至关重要。在糖尿病肾病（DN）中，溶质载体家族7成员11（SLC7A11）高表达和核受体辅激活因子4（NCOA4）低表达与疾病进展有关。对于多囊肾病（PKD），铁死亡通过调节肾组织中的铁死亡促进疾病发展。肾细胞癌（RCC）和狼疮性肾炎（LN）也与铁死亡有关，线粒体DNA和铁蓄积导致RCC，氧化应激导致LN。
铁死亡是一种新发现的程序性细胞死亡形式，与多种疾病相关。它作用于代谢和信号通路，并与AKI、CKD、PKD、DN、LN和透明细胞RCC等肾脏疾病有关。了解其在这些疾病中的作用可能会在其发病机制、病因和治疗方面取得突破。
