Irazabal Maria V, Torres Vicente E
Division of Nephrology and Hypertension, Mayo Clinic, Rochester MN 55905, USA.
Curr Hypertens Rev. 2013 Feb;9(1):44-59. doi: 10.2174/1573402111309010008.
The improvement of imaging techniques over the years has contributed to the understanding of the natural history of autosomal dominant polycystic kidney disease, and facilitated the observation of its structural progression. Advances in molecular biology and genetics have made possible a greater understanding of the genetics, molecular, and cellular pathophysiologic mechanisms responsible for its development and have laid the foundation for the development of potential new therapies. Therapies targeting genetic mechanisms in ADPKD have inherent limitations. As a result, most experimental therapies at the present time are aimed at delaying the growth of the cysts and associated interstitial inflammation and fibrosis by targeting tubular epithelial cell proliferation and fluid secretion by the cystic epithelium. Several interventions affecting many of the signaling pathways disrupted in ADPKD have been effective in animal models and some are currently being tested in clinical trials.
多年来成像技术的进步有助于人们了解常染色体显性多囊肾病的自然病史,并便于观察其结构进展。分子生物学和遗传学的进展使人们能够更深入地了解其发生发展所涉及的遗传学、分子及细胞病理生理机制,并为潜在新疗法的开发奠定了基础。针对常染色体显性多囊肾病遗传机制的疗法存在固有局限性。因此,目前大多数实验性疗法旨在通过针对肾小管上皮细胞增殖及囊性上皮细胞的液体分泌来延缓囊肿生长以及相关的间质炎症和纤维化。在常染色体显性多囊肾病中,有几种干预措施可影响许多被破坏的信号通路,这些措施在动物模型中已取得成效,目前有些正在临床试验中进行测试。