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中国临床药理学与治疗学 ›› 2024, Vol. 29 ›› Issue (3): 348-353.doi: 10.12092/j.issn.1009-2501.2024.03.014

• 综述与讲座 • 上一篇    下一篇

驱动肾小管间质纤维化的新机制

张燕妮,段宇鑫,柏艺,俞瑾瑶,孙佳怡,王泽洁,李玲,叶啟发   

  1. 武汉大学中南医院,武汉大学肝胆疾病研究院,武汉大学移植医学中心,国家人体捐献器官获取质量控制中心,移植医学技术湖北省重点实验室,武汉  430071,湖北

  • 收稿日期:2023-07-07 修回日期:2024-01-29 出版日期:2024-03-26 发布日期:2024-02-29
  • 通讯作者: 李玲,女,博士,副主任药师,研究方向:器官移植术后并发症的个体化基因研究。 E-mail: zn000426@whu.edu.cn
  • 作者简介:张燕妮,女,研究方向:器官移植术后并发症的个体化基因研究。 E-mail: 2020305233147@whu.edu.cn
  • 基金资助:
    2021年湖北省自然科学基金青年基金(2021CFB062);武汉大学基础-临床共建项目培育基金(JCZN2022006);中央高校基本科研业务费专项资金青年教师资助项目(2042023kf0064);2023年武汉大学中南医院转化医学及交叉学科研究联合基金(ZNJC202319)

Novel mechanisms driving renal tubulointerstitial fibrosis

ZHANG Yanni, DUAN Yuxin, BAI Yi, YU Jinyao, SUN Jiayi, WANG Zejie, LI Ling, YE Qifa   

  1. Zhongnan Hospital of Wuhan University, Institute of Hepatobiliary Diseases of Wuhan University, Transplant Center of Wuhan University, National Quality Control Center for Donated Organ Procurement, Hubei Key Laboratory of Medical Technology on Transplantation, Wuhan 430071, Hubei, China 
  • Received:2023-07-07 Revised:2024-01-29 Online:2024-03-26 Published:2024-02-29

摘要:

肾纤维化,尤其是肾小管间质纤维化,是所有慢性肾脏疾病进展为终末期肾病的最常见途径。肾小管上皮细胞在受到慢性损伤后会发生糖脂代谢改变、未折叠蛋白反应、自噬和衰老、上皮细胞-间充质转化和细胞周期G2/M期停滞等几种适应性反应。修复机制适应不良,会诱导产生肾小管间质纤维化。本文将讨论肾小管上皮细胞的这些适应性反应驱动肾小管间质纤维化的分子机制,为探寻肾小管间质纤维化新的药物作用靶点提供参考。

关键词: 慢性肾损伤, 间质纤维化, 肾小管上皮细胞

Abstract:

Renal fibrosis, especially tubulointerstitial fibrosis, is the most common pathway of all chronic kidney diseases progressing to end-stage renal diseases. Several adaptive reactions occur in renal tubular epithelial cells after chronic injury, such as changes in glycolipid metabolism, unfolded protein response, autophagy and senescence, epithelial-to-mesenchymal transition and G2/M cell cycle arrest. Maladaptive repair mechanisms can induce tubulointerstitial fibrosis. This article will discuss the molecular mechanism of these adaptive responses of renal tubular epithelial cells driving renal tubulointerstitial fibrosis, and provide a basis for exploring new drug targets for renal tubulointerstitial fibrosis.

Key words: chronic kidney diseases, tubulointerstitial fibrosis, tubular epithelial cells

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