The crosstalk of Wnt/β-catenin signaling and p53 in acute kidney injury and chronic kidney disease

被引:3
作者
Ming, Wen-Hua [1 ]
Wen, Lin [2 ]
Hu, Wen-Juan [2 ]
Qiao, Rong-Fang [2 ]
Zhou, Yang [3 ]
Su, Bo-Wei [2 ]
Bao, Ya-Nan [2 ]
Gao, Ping [2 ]
Luan, Zhi-Lin [2 ]
机构
[1] Capital Med Univ, Beijing Shijitan Hosp, Dept Allergy, Beijing, Peoples R China
[2] Dalian Med Univ, Adv Inst Med Sci, 9 West Sect,Lvshun South Rd, Dalian 116044, Liaoning, Peoples R China
[3] Beijing Inst Med Device Testing, Beijing, Peoples R China
关键词
Acute kidney injury; Chronic renal insufficiency; Crosstalk; p53; Wnt/beta-catenin; MESENCHYMAL STEM-CELLS; BETA-CATENIN; PODOCYTE APOPTOSIS; TUMOR-SUPPRESSOR; WNT; ACTIVATION; FIBROSIS; PATHWAY; AUTOPHAGY; INHIBITION;
D O I
10.23876/j.krcp.23.344
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Wnt/beta-catenin is a signaling pathway associated with embryonic development, organ formation, cancer, and fibrosis. Its activation can repair kidney damage during acute kidney injury (AKI) and accelerate the occurrence of renal fibrosis after chronic kidney disease (CKD). Interestingly, p53 has also been found as a key modulator in AKI and CKD in recent years. Meantime, some studies have found crosstalk between Wnt/(3-catenin signaling pathways and p53, but more evidence is required on whether they have synergistic effects in renal disease progression. This article reviews the role and therapeutic targets of Wnt/(3-catenin and p53 in AKI and CKD and proposes for the first time that Wnt/(3-catenin and p53 have a synergistic effect in the treatment of renal injury.
引用
收藏
页码:724 / 738
页数:15
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