Department of Biomedical Engineering, Vanderbilt University, Nashville, TN.
Division of Nephrology and Hypertension, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN; Department of Medicine, Veterans Affairs Hospital, Tennessee Valley Healthcare System, Nashville, TN; Department of Cell and Developmental Biology, Vanderbilt University, Nashville, TN.
Semin Nephrol. 2020 Mar;40(2):126-137. doi: 10.1016/j.semnephrol.2020.01.004.
Acute kidney injury (AKI) portends a poor clinical prognosis and increases the risk for the development of chronic kidney disease (CKD). Currently, there are no therapies to treat AKI or prevent its progression to CKD. Wnt/β-catenin is a critical regulator of kidney development that is up-regulated after injury. Most of the literature support a beneficial role for Wnt/β-catenin in AKI, but suggest that this pathway promotes the progression of tubulointerstitial fibrosis, the hallmark of CKD progression. We review the role of Wnt/β-catenin in renal injury with a focus on its potential as a therapeutic target in AKI and in AKI to CKD transition.
急性肾损伤 (AKI) 预示着不良的临床预后,并增加了慢性肾脏病 (CKD) 的发展风险。目前,尚无治疗 AKI 或预防其进展为 CKD 的疗法。Wnt/β-catenin 是肾脏发育的关键调节因子,损伤后会被上调。大多数文献支持 Wnt/β-catenin 在 AKI 中的有益作用,但表明该途径促进了 CKD 进展的标志性肾小管间质纤维化的进展。我们回顾了 Wnt/β-catenin 在肾脏损伤中的作用,重点关注其作为 AKI 治疗靶点以及 AKI 向 CKD 转化中的潜在作用。