Cell Biology, Genzyme Corporation, 49 New York Avenue, Framingham, MA, USA.
Trends Mol Med. 2011 Nov;17(11):625-33. doi: 10.1016/j.molmed.2011.06.003. Epub 2011 Jul 19.
Polycystic kidney diseases (PKDs) comprise a large group of genetic disorders characterized by formation of cysts in the kidneys and other organs, ultimately leading to end-stage renal disease. Although PKDs can be caused by mutations in different genes, they converge on a set of common molecular mechanisms involved in cystogenesis and ciliary dysfunction, and can be qualified as ciliopathies. Recent advances in understanding the mechanisms regulating disease progression have led to the development of new therapies that are being tested in both preclinical and clinical trials. In this article, we briefly review a network of molecular pathways of cystogenesis that are regulated by ciliary functions. We discuss the mTOR pathway in depth, highlighting recent progress in understanding its role in PKD and the current results of clinical trials.
多囊肾病(PKD)是一大类遗传性疾病,其特征是肾脏和其他器官中形成囊肿,最终导致终末期肾病。尽管 PKD 可以由不同基因的突变引起,但它们都集中在一组共同的参与囊肿形成和纤毛功能障碍的分子机制上,可以被定性为纤毛病。最近在理解调节疾病进展的机制方面的进展导致了新疗法的开发,这些疗法正在临床前和临床试验中进行测试。在本文中,我们简要回顾了由纤毛功能调节的囊肿发生的分子途径网络。我们深入讨论了 mTOR 途径,强调了其在 PKD 中的作用以及临床试验的最新结果。