The role of beta-catenin in cyst initiation in Autosomal Dominant Polycystic Kidn

β-连环蛋白在常染色体显性多囊肾囊肿发生中的作用

基本信息

  • 批准号:
    9064636
  • 负责人:
  • 金额:
    $ 38.06万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2014
  • 资助国家:
    美国
  • 起止时间:
    2014-07-28 至 2018-04-30
  • 项目状态:
    已结题

项目摘要

DESCRIPTION (provided by applicant): Autosomal Dominant Polycystic kidney disease (ADPKD) is characterized by numerous cysts within the kidneys of afflicted individuals. The cysts formed in ADPKD can greatly enlarge the kidneys while replacing the normal kidney structures, resulting in reduced kidney function and progression to end-stage renal disease that can only be treated by lifelong dialysis or kidney transplants. As a disease that affects 1 in 800~1000 individuals, ADPKD is among the most common genetic disorders. In the United States, there are 600,000 individuals, and worldwide 12.5 million, with PKD [1]. Thus, ADPKD represents a major public health issue, and accounts for hundreds of millions (and perhaps over a billion) of dollars in health care costs, particularly for dialysis treatments and the cost of drgs that prevent transplant rejections, as well as the cost involved of decreased productivity and impaired quality of life of individuals with ADPKD. For all these reasons, it is of great importanc to discover treatments that directly affect the molecular causes of ADPKD, and that will prevent the progression to end- stage renal disease and dialysis or transplantation. Over the past 5 years the Kreidberg laboratory has investigated the role of receptor tyrosine kinase and Wnt signaling in the pathogenesis of ADPKD. Dr. Kreidberg's laboratory has found that Wnt signaling and beta-catenin expression is highly elevated in cyst lining cells in ADPKD. In this grant they propose to extend their studies to understand how b-catenin integrates signals from many pathways to cause the initiation of cyst formation in individuals with ADPKD. By understanding the processes involved in the initiation of cysts, we may identify therapeutic targets that inhibit the initiation or early progression of cysts, before they are clinically detectable.
描述(由申请人提供):常染色体显性遗传性多囊肾病(ADPKD)的特征是患者的肾脏内有大量的囊肿。ADPKD中形成的囊变可使肾脏大大增大,同时取代正常的肾脏结构,导致肾功能下降,进展为终末期肾脏疾病,只能通过终生透析或肾移植来治疗。ADPKD是一种每800~1000人中就有1人患病的疾病,是最常见的遗传病之一。在美国,有60万人患有PKD,全世界有1250万人[1]。因此,ADPKD是一个重大的公共卫生问题,占医疗保健费用的数亿美元(或许超过10亿美元),特别是用于透析治疗的费用和防止移植排斥反应的DRGs费用,以及ADPKD患者生产力下降和生活质量受损的费用。因此,寻找直接影响ADPKD分子病因的治疗方法,防止进展为终末期肾病和透析或移植是非常重要的。在过去的5年里,Kreidberg实验室研究了受体酪氨酸激酶和Wnt信号在ADPKD发病机制中的作用。Kreidberg博士的实验室发现,在ADPKD的囊壁细胞中,Wnt信号和β-catenin的表达高度升高。在这项授权中,他们建议扩展他们的研究,以了解b-catenin如何整合来自许多途径的信号,从而导致ADPKD患者的囊性形成。通过了解囊性病变的发生过程,我们可以在临床可察觉之前,确定抑制囊肿性病变发生或早期进展的治疗靶点。

项目成果

期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)

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Jordan A Kreidberg其他文献

KIDNEY AND LUNG ABNORMALITIES IN α-3 INTEGRIN DEFICIENT MICE. † 338
α-3 整合素缺陷小鼠的肾脏和肺部异常。†338
  • DOI:
    10.1203/00006450-199604001-00358
  • 发表时间:
    1996-04-01
  • 期刊:
  • 影响因子:
    3.100
  • 作者:
    Stuart L Goldstein;Michael J Donovan;Jordan A Kreidberg
  • 通讯作者:
    Jordan A Kreidberg

Jordan A Kreidberg的其他文献

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{{ truncateString('Jordan A Kreidberg', 18)}}的其他基金

The Role of Fibronectin in ADPKD
纤连蛋白在 ADPKD 中的作用
  • 批准号:
    10217127
  • 财政年份:
    2019
  • 资助金额:
    $ 38.06万
  • 项目类别:
The Role of Fibronectin in ADPKD
纤连蛋白在 ADPKD 中的作用
  • 批准号:
    10021645
  • 财政年份:
    2019
  • 资助金额:
    $ 38.06万
  • 项目类别:
Transcriptional Reprogramming in Podocyte Injury
足细胞损伤中的转录重编程
  • 批准号:
    9149798
  • 财政年份:
    2016
  • 资助金额:
    $ 38.06万
  • 项目类别:
The role of beta-catenin in cyst initiation in Autosomal Dominant Polycystic Kidn
β-连环蛋白在常染色体显性多囊肾囊肿发生中的作用
  • 批准号:
    8683329
  • 财政年份:
    2014
  • 资助金额:
    $ 38.06万
  • 项目类别:
Misregulation of receptor tyrosine kinase signaling in PKD
PKD 中受体酪氨酸激酶信号传导的失调
  • 批准号:
    8338906
  • 财政年份:
    2011
  • 资助金额:
    $ 38.06万
  • 项目类别:
Misregulation of receptor tyrosine kinase signaling in PKD
PKD 中受体酪氨酸激酶信号传导的失调
  • 批准号:
    8726973
  • 财政年份:
    2011
  • 资助金额:
    $ 38.06万
  • 项目类别:
Misregulation of receptor tyrosine kinase signaling in PKD
PKD 中受体酪氨酸激酶信号传导的失调
  • 批准号:
    8238482
  • 财政年份:
    2011
  • 资助金额:
    $ 38.06万
  • 项目类别:
Misregulation of receptor tyrosine kinase signaling in PKD
PKD 中受体酪氨酸激酶信号传导的失调
  • 批准号:
    8541009
  • 财政年份:
    2011
  • 资助金额:
    $ 38.06万
  • 项目类别:
BMP and FGF Signaling in kidney progenitor cells
肾祖细胞中的 BMP 和 FGF 信号转导
  • 批准号:
    8494042
  • 财政年份:
    2010
  • 资助金额:
    $ 38.06万
  • 项目类别:
BMP and FGF Signaling in kidney progenitor cells
肾祖细胞中的 BMP 和 FGF 信号转导
  • 批准号:
    8318882
  • 财政年份:
    2010
  • 资助金额:
    $ 38.06万
  • 项目类别:

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