TY - JOUR
T1 - P53 in kidney injury and repair
T2 - Mechanism and therapeutic potentials
AU - Tang, Chengyuan
AU - Ma, Zhengwei
AU - Zhu, Jiefu
AU - Liu, Zhiwen
AU - Liu, Yuxue
AU - Liu, Yu
AU - Cai, Juan
AU - Dong, Zheng
N1 - Funding Information:
This study was supported partly by the grants from National Natural Science Foundation of China ( 81720108008, 81870474 , 81430017 ), the National Institutes of Health of USA, and Department of Veterans Administration of USA.
Publisher Copyright:
© 2018 Elsevier Inc.
PY - 2019/3
Y1 - 2019/3
N2 - Acute kidney injury (AKI) is a major kidney disease with poor clinical outcome. Besides its acute consequence of high mortality, AKI may also contribute significantly to the occurrence and progression of chronic kidney diseases (CKD). Accumulating evidence has demonstrated that maladaptive and incomplete kidney repair after AKI leads to the development of renal fibrosis and, ultimately, CKD. p53, a well-known tumor suppressor, plays a critical role in AKI and subsequent kidney repair through the regulation of various cell biologic processes, including apoptosis, cell cycle arrest, and autophagy. Despite the notable progress in deciphering the involvement of p53 in kidney injury and repair, the underlying mechanisms of p53 in these pathological processes remain largely unknown. Further investigation in this area is essential for the application of p53 as therapeutic target to prevent and treat AKI or impede its progression to CKD. In this review, we summarize the recent advances in understanding p53 regulation of AKI and kidney repair, pinpoint the potential of p53 as a therapeutic target, and present future research interests and directions.
AB - Acute kidney injury (AKI) is a major kidney disease with poor clinical outcome. Besides its acute consequence of high mortality, AKI may also contribute significantly to the occurrence and progression of chronic kidney diseases (CKD). Accumulating evidence has demonstrated that maladaptive and incomplete kidney repair after AKI leads to the development of renal fibrosis and, ultimately, CKD. p53, a well-known tumor suppressor, plays a critical role in AKI and subsequent kidney repair through the regulation of various cell biologic processes, including apoptosis, cell cycle arrest, and autophagy. Despite the notable progress in deciphering the involvement of p53 in kidney injury and repair, the underlying mechanisms of p53 in these pathological processes remain largely unknown. Further investigation in this area is essential for the application of p53 as therapeutic target to prevent and treat AKI or impede its progression to CKD. In this review, we summarize the recent advances in understanding p53 regulation of AKI and kidney repair, pinpoint the potential of p53 as a therapeutic target, and present future research interests and directions.
KW - Acute kidney injury
KW - Apoptosis
KW - Autophagy
KW - Cell cycle
KW - Kidney repair
KW - Renal fibrosis
KW - p53
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U2 - 10.1016/j.pharmthera.2018.10.013
DO - 10.1016/j.pharmthera.2018.10.013
M3 - Review article
C2 - 30347214
AN - SCOPUS:85055173334
VL - 195
SP - 5
EP - 12
JO - Pharmacology and Therapeutics, Part A: Chemotherapy, Toxicology and
JF - Pharmacology and Therapeutics, Part A: Chemotherapy, Toxicology and
SN - 0163-7258
ER -