Department of Biomedical Science and Physiology, Faculty of Science and Engineering, University of Wolverhampton, Wulfruna Street, Wolverhampton WV1 1LY, UK.
Genes (Basel). 2020 Apr 30;11(5):496. doi: 10.3390/genes11050496.
Chronic kidney disease (CKD) encompasses a group of diverse diseases that are associated with accumulating kidney damage and a decline in glomerular filtration rate (GFR). These conditions can be of an acquired or genetic nature and, in many cases, interactions between genetics and the environment also play a role in disease manifestation and severity. In this review, we focus on genetically inherited chronic kidney diseases and dissect the links between canonical and non-canonical Wnt signalling, and this umbrella of conditions that result in kidney damage. Most of the current evidence on the role of Wnt signalling in CKD is gathered from studies in polycystic kidney disease (PKD) and nephronophthisis (NPHP) and reveals the involvement of beta-catenin. Nevertheless, recent findings have also linked planar cell polarity (PCP) signalling to CKD, with further studies being required to fully understand the links and molecular mechanisms.
慢性肾脏病（CKD）涵盖了一组不同的疾病，这些疾病与肾脏损伤的积累和肾小球滤过率（GFR）的下降有关。这些疾病可能是后天获得的，也可能是遗传的，在许多情况下，遗传和环境之间的相互作用也在疾病的表现和严重程度中发挥作用。在这篇综述中，我们专注于遗传性慢性肾脏病，并剖析经典和非经典 Wnt 信号通路与导致肾脏损伤的这一类病症之间的联系。目前关于 Wnt 信号通路在 CKD 中的作用的大部分证据来自多囊肾病（PKD）和肾单位肾痨（NPHP）的研究，并揭示了β-连环蛋白的参与。然而，最近的研究结果还将平面细胞极性（PCP）信号通路与 CKD 联系起来，需要进一步的研究来全面了解这些联系和分子机制。
