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易香伶, 何娅妮, 陈客宏. 肾小管上皮细胞应激性衰老在糖尿病肾病中的研究进展[J]. koko体育app 学报(医学版), 2023, 54(6): 1085-1090. DOI:
引用本文: 易香伶, 何娅妮, 陈客宏. 肾小管上皮细胞应激性衰老在糖尿病肾病中的研究进展[J]. koko体育app 学报(医学版), 2023, 54(6): 1085-1090. DOI:
YI Xiangling, HE Yani, CHEN Kehong. Research Progress in Stress-Induced Senescence of Renal Tubular Cells in Diabetic Nephropathy[J]. Journal of Sichuan University (Medical Sciences), 2023, 54(6): 1085-1090. DOI:
Citation: 🌼 YI Xiangling, HE Yani, CHEN Kehong. Research Progress in Stress-Induced Senescence of Renal Tubular Cells in Diabetic Nephropathy[J]. Journal of Sichuan University (Medical Sciences), 2023, 54(6): 1085-1090. DOI:

肾小管上皮细胞应激性衰老在糖尿病肾病中的研究进展

Research Progress in Stress-Induced Senescence of Renal Tubular Cells in Diabetic Nephropathy

  • 摘要: 糖尿病肾病(diabetic nephropathy, DN)是导致终末期肾脏疾病的首要病因。肾小管间质损伤是DN进展为终末期肾脏疾病的重要病理生理基础。肾小管上皮细胞应激性衰老是引起肾小管间质损伤的关键环节。近年来,研究发现肾小管上皮细胞中的内质网、线粒体及溶酶体等细胞器在DN中受到不同程度的损伤,并且它们的功能失衡可以通过引起肾小管上皮细胞应激性衰老导致细胞和组织器官的持续损伤,进而推动疾病进展。然而目前DN中肾小管上皮细胞应激性衰老导致衰老微环境变化的核心机制尚不清楚,且其细胞器失去稳态的发生机制尚待进一步研究。 本综述总结了DN背景下的肾小管损伤、肾小管上皮细胞应激性衰老及其与细胞器的特定病理生理机制,以便为下一步研究以及开发新治疗策略提供参考。  
    Abstract: Diabetic nephropathy (DN) is the leading cause of end-stage renal disease. Renal tubulointerstitial injury is an important pathophysiological basis that contributes to the progression of DN to end-stage renal disease. Stress-induced senescence of renal tubular epithelial cells (RTECs) forms a key link that causes tubulointerstitial injury. In recent years, it has been reported that organelles, such as endoplasmic reticulum, mitochondria, and lysosomes, in RTECs are damaged to varying degrees in DN, and that their functional imbalance may lead to stress-induced senescence of RTECs, thereby causing sustained cellular and tissue-organ damage, which in turn promotes the progression of the disease. However, the core mechanism underlying changes in the senescence microenvironment caused by stress-induced senescence of RTECs in DN is still not understood. In addition, the mechanism by which organelles lose homeostasis also needs to be further investigated. Herein, we described the specific pathophysiological mechanisms of renal tubular injury, stress-induced senescence of RTECs, and their association with organelles in the context of DN in order to provide reference for the next-step research, as well as the development of new therapeutic strategies.  
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