期刊
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
卷 315, 期 4, 页码 F1098-F1106出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajprenal.00199.2018
关键词
acute kidney injury; chronic kidney disease; cisplatin; fibrosis; ischemia; model; nephrotoxicity
资金
- National Natural Science Foundation of China [81720108008, 81430017]
- National Institutes of Health
- Department of Veterans Administration
- Senior Research Career Scientist of Department of Veterans Administration
Acute kidney injury (AKI) is a contributing factor in the development and progression of chronic kidney disease (CKD). Despite rapid progresses, the mechanism underlying AKI-CKD transition remains largely unclear. Animal models recapitulating this process are crucial to the research of the pathophysiology of AKI-CKD transition and the development of effective therapeutics. In this review, we present the commonly used rodent models of AKI-CKD transition, including bilateral ischemia-reperfusion injury (IRI), unilateral IRI, unilateral IRI with contralateral nephrectomy, multiple episodes of IRI, and repeated treatment of low-dose cisplatin, diphtheria toxin, aristolochic acid, or folic acid. The main merits and pitfalls of these models are also discussed. This review provides helpful information for establishing reliable and clinically relevant models for studying post-AKI development of chronic renal pathologies and the progression to CKD.
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