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中华肾病研究电子杂志

中华肾病研究电子杂志 ›› 2026, Vol. 15 ›› Issue (05) : 267 -273. doi: 10.3877/cma.j.issn.2095-3216.2026.05.004

综述

慢性肾脏病中程序性细胞死亡机制的作用研究进展
张雅宁1,2, 郑颖1,2,†()   
  1. 1100853　北京，解放军总医院第一医学中心肾脏病医学部、肾脏疾病全国重点实验室、肾病与泌尿系统疾病国家临床医学研究中心、重症肾脏疾病器械与中西医药物研发北京市重点实验室、数智中医泛血管疾病防治北京市重点实验室、国家中医药管理局高水平中医药重点学科(zyyzdxk-2023310)、国家中医药管理局中医药创新团队及人才支持计划项目(ZYYCXTD-D-202402)
    2100853　北京，解放军医学院
  • 收稿日期:2025-10-13 出版日期:2026-10-28
  • 通信作者: 郑颖
  • 基金资助:
    北京市自然科学基金-大兴创新联合基金资助(L246040)

Research progress on the role of programmed cell death mechanisms in chronic kidney disease

Yaning Zhang1,2, Ying Zheng1,2,†()   

  1. 1Senior Department of Nephrology, First Medical Center of Chinese PLA General Hospital, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney and Urological Diseases, Beijing Key Laboratory of Medical Devices and Integrated Traditional Chinese and Western Drug Development for Severe Kidney Diseases, Beijing Key Laboratory of Digital Intelligent TCM for the Preventionand Treatment of Pan-vascular Diseases, Key Disciplines of National Administration of Traditional Chinese Medicine(zyyzdxk-2023310), Innovation Team and Talents Cultivation Program of National Administration of Traditional Chinese Medicine (ZYYCXTD-D-202402), Beijing 100853, China
    2Chinese PLA Medical School; Beijing 100853, China
  • Received:2025-10-13 Published:2026-10-28
  • Corresponding author: Ying Zheng
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引用本文：

张雅宁, 郑颖. 慢性肾脏病中程序性细胞死亡机制的作用研究进展[J/OL]. 中华肾病研究电子杂志, 2026, 15(05): 267-273.

Yaning Zhang, Ying Zheng. Research progress on the role of programmed cell death mechanisms in chronic kidney disease[J/OL]. Chinese Journal of Kidney Disease Investigation(Electronic Edition), 2026, 15(05): 267-273.

程序性细胞死亡(programmed cell death，PCD)的异常激活在肾脏损伤及纤维化进程中发挥关键调控作用，不同PCD方式可通过多样病理机制参与慢性肾脏病(chronic kidney disease，CKD)发生发展。自噬具有"双刃剑"效应，其适度激活能通过清除受损细胞器与错误折叠蛋白，维持细胞稳态，延缓肾纤维化；而其过度激活或功能受损会造成有害物质累积与线粒体功能障碍，进而加速肾脏疾病进展。坏死性凋亡通过受体相互作用蛋白激酶1/3(receptorinteracting protein kinase 1/3，RIPK1/RIPK3)混合谱系激酶结构域样蛋白(mixed lineage kinase domainlike protein，MLKL)信号通路介导炎症反应，促进肾纤维化。细胞焦亡依赖核苷酸结合寡聚化结构域样受体热蛋白结构域相关蛋白3(nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing protein 3，NLRP3)炎性小体的激活，导致促炎因子释放，加剧肾损伤。铁死亡通过脂质过氧化和铁依赖性机制参与CKD的病理过程。针对上述PCD的靶向治疗策略，已在糖尿病肾脏病、单侧输尿管梗阻、5/6肾切除及急性肾损伤等不同临床前模型中展现出潜在的肾保护效应。本文综述了4种PCD方式在CKD中的作用、机制及其交互作用。未来可借助机器学习优化多靶点联合治疗(如槲皮素衍生物协同调控铁死亡和坏死性凋亡)，实现患者分层与疗效预测，为CKD精准干预提供新范式。

关键词: 慢性肾脏病, 程序性细胞死亡, 炎症, 肾纤维化

Abnormal activation of programmed cell death (PCD) plays a key regulatory role in the progression of kidney injury and fibrosis, and different modes of PCD can participate in the occurrence and development of chronic kidney disease (CKD) through diverse pathological mechanisms. Autophagy has a "double-edged sword" effect. Its moderate activation can maintain cellular homeostasis and retard renal fibrosis by clearing damaged organelles and misfolded proteins. However, its excessive activation or impaired function leads to the accumulation of harmful substances and mitochondrial dysfunction, thereby accelerating the progression of kidney diseases. Necroptosis mediates inflammatory responses and promotes renal fibrosis via the receptor-interacting protein kinases 1/3 (RIPK1/RIPK3)-mixed lineage kinase domain-like protein (MLKL) signaling pathway. Pyroptosis relies on the activation of the nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing protein 3 (NLRP3) inflammasome, which promotes the release of pro-inflammatory factors and aggravates renal injury. Ferroptosis participates in the pathological process of CKD through lipid peroxidation and iron-dependent mechanisms. Targeted therapeutic strategies for the aforementioned PCD have exhibited potential renal-protective effects in various preclinical models, including diabetic kidney disease, unilateral ureteral obstruction, 5/6 nephrectomy, and acute kidney injury. This paper reviews the roles, mechanisms and interactions of the four PCD modalities in CKD. In the future, machine learning can be leveraged to optimize multi-target combination therapies (e.g., quercetin derivatives synergistically regulating ferroptosis and necroptosis), realize patients stratification and therapeutic effect prediction, and provide a new paradigm for precise intervention of CKD.

Key words: Chronic kidney disease, Programmed cell death, Inflammation, Renal fibrosis
表1 自噬的关键步骤及主要调控分子
步骤及主要调控分子 核心事件 关键分子 主要功能
1.诱导自噬 感知应激信号，解除自噬抑制 mTORC1
AMPK
ULK1复合物		 mTORC1：营养/能量充足时抑制自噬
AMPK：能量不足时激活，抑制mTORC1并激活ULK1
ULK1复合物：自噬启动的核心开关
2.自噬体形成 隔离膜成核、延伸，包裹待降解物并闭合 Ⅲ型PI3K复合物
Atg12-Atg5-Atg16L1系统LC3系统
货物受体(如p62)		 Ⅲ型PI3K复合物：决定膜成核位点
Atg12-Atg5-Atg16L1系统：驱动膜延伸
LC3系统：自噬体膜标志物，介导货物识别
p62：接头蛋白，连接泛素化货物与LC3
3.运输与融合 自噬体运输，与溶酶体融合 Rab7
HOPS复合物
SNARE蛋白(如STX17)		 Rab7：调控自噬体成熟与运输
HOPS复合物：介导膜拴系与对接
SNARE蛋白：催化膜融合
4.完成自噬 内容物降解，产物输出再利用。 溶酶体水解酶(如组织蛋白酶)
溶酶体膜转运蛋白		 水解酶：在酸性下降解大分子
膜转运蛋白：输出氨基酸、脂肪酸等供再利用
核心调控枢纽 整合信号，决定自噬强度 mTOR信号通路
AMPK信号通路		 mTOR通路：主要抑制信号
AMPK通路：主要激活信号。两者拮抗，精细调控
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