TY - JOUR
T1 - Rodent models of AKI and AKI-CKD transition
T2 - an update in 2024
AU - Fu, Ying
AU - Xiang, Yu
AU - Wei, Qingqing
AU - Ilatovskaya, Daria
AU - Dong, Zheng
N1 - Publisher Copyright:
© 2024 American Physiological Society. All rights reserved.
PY - 2024/4
Y1 - 2024/4
N2 - Despite known drawbacks, rodent models are essential tools in the research of renal development, physiology, and pathogenesis. In the past decade, rodent models have been developed and used to mimic different etiologies of acute kidney injury (AKI), AKI to chronic kidney disease (CKD) transition or progression, and AKI with comorbidities. These models have been applied for both mechanistic research and preclinical drug development. However, current rodent models have their limitations, especially since they often do not fully recapitulate the pathophysiology of AKI in human patients, and thus need further refinement. Here, we discuss the present status of these rodent models, including the pathophysiologic compatibility, clinical translational significance, key factors affecting model consistency, and their main limitations. Future efforts should focus on establishing robust models that simulate the major clinical and molecular phenotypes of human AKI and its progression.
AB - Despite known drawbacks, rodent models are essential tools in the research of renal development, physiology, and pathogenesis. In the past decade, rodent models have been developed and used to mimic different etiologies of acute kidney injury (AKI), AKI to chronic kidney disease (CKD) transition or progression, and AKI with comorbidities. These models have been applied for both mechanistic research and preclinical drug development. However, current rodent models have their limitations, especially since they often do not fully recapitulate the pathophysiology of AKI in human patients, and thus need further refinement. Here, we discuss the present status of these rodent models, including the pathophysiologic compatibility, clinical translational significance, key factors affecting model consistency, and their main limitations. Future efforts should focus on establishing robust models that simulate the major clinical and molecular phenotypes of human AKI and its progression.
KW - cisplatin nephrotoxicity
KW - renal ischemia-reperfusion
KW - rhabdomyolysis
KW - rodent model
KW - sepsis
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U2 - 10.1152/ajprenal.00402.2023
DO - 10.1152/ajprenal.00402.2023
M3 - Review article
C2 - 38299215
AN - SCOPUS:85188480098
SN - 1931-857X
VL - 326
SP - F563-F583
JO - American Journal of Physiology - Renal Physiology
JF - American Journal of Physiology - Renal Physiology
IS - 4
ER -