• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

多囊肾病:从床边到基因再回归临床

Polycystic kidney disease: from the bedside to the gene and back.

作者信息

Grantham J J

机构信息

Department of Internal Medicine, Biochemistry and Molecular Biology, Kidney Institute, Kansas University Medical Center, Kansas City, Kansas, USA.

出版信息

Curr Opin Nephrol Hypertens. 2001 Jul;10(4):533-42. doi: 10.1097/00041552-200107000-00008.

DOI:10.1097/00041552-200107000-00008
PMID:11458035
Abstract

Collated in this highly personal commentary are the most important research findings of the past 10 years that deal primarily with the renal manifestations of inherited polycystic kidney diseases. Progress in understanding these complex disorders has followed two major concurrent and convergent lines of investigation: genes and genetic mechanisms, and pathogenesis and progression. The field has moved from descriptive pathobiology to the elucidation of molecular mechanisms consequent to genetic and epigenetic events. Doubtless, the favorite works of some who have labored diligently in this field have not been fully exalted, and for this I apologize. Were I the editor, this entire celebratory volume would be used to extol the thrilling growth of knowledge during the tenure of this polycystic kidney disease watcher.

摘要

在这篇极具个人色彩的评论中,整理了过去10年中最重要的研究发现,这些发现主要涉及遗传性多囊肾病的肾脏表现。在理解这些复杂疾病方面的进展遵循了两条主要的并行且趋同的研究路线:基因与遗传机制,以及发病机制与疾病进展。该领域已从描述性病理生物学转向对基因和表观遗传事件导致的分子机制的阐释。毫无疑问,一些在该领域辛勤耕耘的人的杰出作品尚未得到充分颂扬,为此我表示歉意。如果我是编辑,这本整本的庆祝文集将用来赞颂在这位多囊肾病观察者任职期间知识的惊人增长。

相似文献

1
Polycystic kidney disease: from the bedside to the gene and back.多囊肾病:从床边到基因再回归临床
Curr Opin Nephrol Hypertens. 2001 Jul;10(4):533-42. doi: 10.1097/00041552-200107000-00008.
2
Molecular mechanisms of polycystic kidney disease.多囊肾病的分子机制
Biochim Biophys Acta. 2011 Oct;1812(10):1201. doi: 10.1016/j.bbadis.2011.08.004.
3
Recent advances in the understanding of polycystic kidney disease.多囊肾病认识方面的最新进展。
Curr Opin Nephrol Hypertens. 1997 Jul;6(4):377-83. doi: 10.1097/00041552-199707000-00012.
4
An Overview of In Vivo and In Vitro Models for Autosomal Dominant Polycystic Kidney Disease: A Journey from 3D-Cysts to Mini-Pigs.常染色体显性遗传多囊肾病体内和体外模型概述:从 3D 囊肿到迷你猪。
Int J Mol Sci. 2020 Jun 25;21(12):4537. doi: 10.3390/ijms21124537.
5
The Jeremiah Metzger Lecture. Polycystic kidney disease: old disease in a new context.杰里迈亚·梅茨格讲座。多囊肾病:新背景下的古老疾病。
Trans Am Clin Climatol Assoc. 2002;113:211-24; discussion 224-6.
6
[Polycystic kidney diseases: molecular genetics and counselling].[多囊肾病:分子遗传学与遗传咨询]
Nephrol Ther. 2006 Jul;2(3):120-6. doi: 10.1016/j.nephro.2006.03.001. Epub 2006 Jun 27.
7
Is autophagy the culprit of cystogenesis in polycystic kidney disease?自噬是多囊肾病中囊肿形成的罪魁祸首吗?
EBioMedicine. 2020 Nov;61:103043. doi: 10.1016/j.ebiom.2020.103043. Epub 2020 Oct 7.
8
The molecular biology of polycystic kidney disease.多囊肾病的分子生物学
Pediatr Nephrol. 1998 Nov;12(9):721-6. doi: 10.1007/s004670050534.
9
The expression of somatostatin receptor 2 decreases during cyst growth in mice with polycystic kidney disease.在多囊肾病小鼠的囊肿生长过程中,生长抑素受体 2 的表达减少。
Exp Biol Med (Maywood). 2018 Sep;243(13):1092-1098. doi: 10.1177/1535370218803893. Epub 2018 Sep 27.
10
Polycystic kidney disease: SMYD2 is a novel epigenetic regulator of cyst growth.多囊肾病:SMYD2是囊肿生长的一种新型表观遗传调节因子。
Nat Rev Nephrol. 2017 Sep;13(9):513. doi: 10.1038/nrneph.2017.99. Epub 2017 Jul 3.

引用本文的文献

1
Long-Term Effects of Tolvaptan Therapy on Total Kidney Volume and Renal Function in Patients with Autosomal Dominant Polycystic Kidney Disease: A Single-Center Experience.托伐普坦治疗常染色体显性多囊肾病患者对总肾体积和肾功能的长期影响:单中心经验
J Clin Med. 2025 Sep 17;14(18):6537. doi: 10.3390/jcm14186537.
2
Co-Inheritance of Pathogenic Variants in and Genes Determined by Parental Segregation and De Novo Origin: A Case Report.致病变异在 和 基因中的共遗传,通过父母遗传分离和新生起源确定:病例报告。
Genes (Basel). 2023 Aug 6;14(8):1589. doi: 10.3390/genes14081589.
3
Automated prognosis of renal function decline in ADPKD patients using deep learning.
利用深度学习技术对 ADPKD 患者肾功能下降进行自动预测。
Z Med Phys. 2024 May;34(2):330-342. doi: 10.1016/j.zemedi.2023.08.001. Epub 2023 Aug 21.
4
Massive bilateral polycystic kidneys, successful treatment with embolization and nephrectomy: A case report.巨大双侧多囊肾,经栓塞及肾切除术成功治疗:一例报告
Urol Case Rep. 2023 May 3;48:102422. doi: 10.1016/j.eucr.2023.102422. eCollection 2023 May.
5
Deep Learning-Based Total Kidney Volume Segmentation in Autosomal Dominant Polycystic Kidney Disease Using Attention, Cosine Loss, and Sharpness Aware Minimization.基于深度学习的常染色体显性多囊肾病全肾体积分割:使用注意力机制、余弦损失和锐度感知最小化
Diagnostics (Basel). 2022 May 7;12(5):1159. doi: 10.3390/diagnostics12051159.
6
The correlation between kidney volume and measured glomerular filtration rate in an Asian ADPKD population: a prospective cohort study.亚洲多囊肾病患者肾脏体积与肾小球滤过率测定值的相关性:一项前瞻性队列研究。
BMC Nephrol. 2021 May 15;22(1):178. doi: 10.1186/s12882-021-02392-0.
7
Disrupting polycystin-2 EF hand Ca affinity does not alter channel function or contribute to polycystic kidney disease.破坏多囊蛋白-2 EF 手钙离子亲和力不会改变通道功能,也不会导致多囊肾病。
J Cell Sci. 2020 Dec 24;133(24):jcs255562. doi: 10.1242/jcs.255562.
8
Structure and function of polycystin channels in primary cilia.原发性纤毛中多囊蛋白通道的结构与功能。
Cell Signal. 2020 Aug;72:109626. doi: 10.1016/j.cellsig.2020.109626. Epub 2020 Apr 3.
9
Primary cilia and the exocyst are linked to urinary extracellular vesicle production and content.原发性纤毛和外被体与尿细胞外囊泡的产生和内容有关。
J Biol Chem. 2019 Dec 13;294(50):19099-19110. doi: 10.1074/jbc.RA119.009297. Epub 2019 Nov 6.
10
Polycystin-2 is an essential ion channel subunit in the primary cilium of the renal collecting duct epithelium.多囊蛋白-2 是肾脏集合管上皮初级纤毛中的重要离子通道亚基。
Elife. 2018 Feb 14;7:e33183. doi: 10.7554/eLife.33183.