Regulatory Pathways of Cell Apoptosis in Diabetic Kidney Disease and Intervention by Traditional Chinese Medicine： A Review
10.13422/j.cnki.syfjx.20252063
- VernacularTitle:糖尿病肾脏病细胞凋亡的调控途径及中医药干预研究进展
- Author:
Yunjie YANG
1
;
Mingqian JIANG
1
;
Chen QIU
1
;
Yaqing RUAN
1
;
Senlin CHEN
2
;
Wenxin HUANG
2
;
Hangbin ZHENG
2
;
Yi WEI
3
;
Pengfei LI
1
;
Xueqin LIN
1
;
Jing WU
1
;
Shiwei RUAN
1
;
Jianting WANG
1
;
Yuliang QIU
1
Author Information
1. Fujian Provincial People's Hospital，Fuzhou 350004，China
2. The First Clinical Medical College of Fujian University of Traditional Chinese Medicine，Fuzhou 350004，China
3. The Fourth Clinical Medical College of Guangzhou University of Chinese Medicine，Shenzhen 518033，China
- Publication Type:Journal Article
- Keywords:
diabetic kidney disease;
apoptosis;
signaling pathways;
mitochondria;
endoplasmic reticulum;
traditional Chinese medicine;
mechanism
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2026;32(9):294-306
- CountryChina
- Language:Chinese
-
Abstract:
Diabetic kidney disease（DKD） is a chronic kidney structural and functional disorder caused by diabetes. With the global prevalence of diabetes continuing to rise， DKD has gradually become a major cause of chronic kidney disease and end-stage renal disease（ESRD）， posing a serious threat to patients' quality of life and long-term health outcomes. Studies have shown that apoptosis plays a pivotal role in the development and progression of DKD， with its mechanisms involving abnormal activation of multiple signaling pathways such as Toll-like receptor 4（TLR4）/nuclear transcription factor-κB（NF-κB）/B-cell lymphoma-2（Bcl-2）/cysteinyl aspartate-specific proteinase（Caspase）-3， protein kinase R-like endoplasmic reticulum kinase（PERK）/eukaryotic initiation factor 2α（eIF2α）/activating transcript factor 4（ATF4）/CCAAT enhancer-binding protein homologous protein（CHOP）， phosphatidylinositol 3-kinase（PI3K）/protein kinase B（Akt）/glycogen synthase kinase-3β（GSK-3β）， Janus kinase 2（JAK2）/signal transducer and activator of transcription 3（STAT3）， adenosine monophosphate-activated protein kinase（AMPK）/mammalian target of rapamycin（mTOR） and silent information regulator 1（SIRT1）/tumor suppressor protein 53（p53）， thereby accelerating renal pathological damage in DKD. Extensive evidence-based medical studies have confirmed that traditional Chinese medicine（TCM）， leveraging its unique therapeutic advantages of multi-target， multi-component and multi-pathway approaches， has demonstrated remarkable efficacy and favorable safety profiles in treating DKD. Recent studies have demonstrated that active components of TCM can specifically target and modulate key effectors in apoptotic signaling pathways. Meanwhile， traditional compound formulations exert synergistic effects through multiple approaches such as replenishing deficiency and activating blood circulation， detoxifying and dredging collaterals， tonifying kidney essence， and removing stasis and purging turbidity， thereby comprehensively regulating critical pathological processes including endoplasmic reticulum stress and mitochondrial apoptosis pathways. This combined therapeutic approach of molecular targeting and holistic regulation provides novel strategies for delaying the progression of DKD. Based on this， this paper provides an in-depth analysis of key apoptotic signaling pathways and their regulatory mechanisms， while systematically summarizing recent research advances regarding the therapeutic effects of TCM active components， compound formulations， and proprietary Chinese medicines on DKD through modulation of these pathways， with particular emphasis on their underlying molecular mechanisms. These findings not only elucidate the modern scientific connotation and theoretical basis of TCM in treating DKD but also establish a solid theoretical and practical foundation for promoting the wider clinical application and further research of TCM in the field of DKD treatment.
