Elucidating hallmarks of aging in the development of lower urinary tract dysfunction (LUTD)

阐明下尿路功能障碍 (LUTD) 发展中的衰老特征

基本信息

  • 批准号:
    10684318
  • 负责人:
  • 金额:
    $ 58.47万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2021
  • 资助国家:
    美国
  • 起止时间:
    2021-09-24 至 2025-08-31
  • 项目状态:
    未结题

项目摘要

ABSTRACT Aging is the single largest risk factor for many common diseases that burden public health. This is especially true in the prostate. The prostate is a male sex accessory gland that is important in reproduction. However, as men age the prostate undergoes a prototypical aging change, fibrosis. The aged fibrotic prostate causes urinary symptoms which will afflict nearly every man if they live long enough. Our team has led an effort to define the aged prostate and its associated urinary symptoms in overall health. To date aging mechanisms have not been thoroughly tested or targeted for the nonmalignant prostate. Rather androgen regulated pathways and alpha adrenergic activity have dominated the field. The long-term goal of this application is to better understand how mitochondrial dysfunction and related molecular and cellular mechanisms promote prostate aging and fibrosis, ultimately leading to prostate dysfunction, urinary symptoms and overall poor health. Mitochondrial dysfunction has become an accepted mechanism of aging. However, the role of mitochondrial dysfunction in the prostate has not been thoroughly tested. In part this is because there is little understanding of the role of mitochondria in prostate function and no models have been identified to test it. To better understand the role of mitochondrial dysfunction in the aging prostate, we will perform 4 Aims. Aim 1 will assess the gain of prostatic mitochondrial dysfunction using chemical inhibitors of mitochondrial complex I of the electron transport chain and determine if prostatic aging is accelerated ultimately leading to a dysfunctional prostate. Aim 2 will determine the molecular mechanism by which mitochondrial dysfunction induces aging and fibrosis. Aim 3 identifies the localization of mitochondrial dysfunction in specific cells and anatomical areas of the prostate of men, including differences in race as well as in the lower urinary tract of mice. Aim 4 tests the effectiveness of pro-mitochondrial health drugs in reversing mitochondrial dysfunction, prostate aging, and urinary dysfunction in human and mouse models of aging. Identifying pharmacological age related interventions in novel prostate aging animal models to improve mitochondrial homeostasis would be highly desirable towards the goal of prolonging healthspan. The potential translational impact of this approach is high, as the proposed senolytics are already FDA approved and can be rapidly included into clinical trials. Upon the completion of this work, we will better understand the role of mitochondrial dysfunction in the aging prostate and how to target this pathway for better urinary and overall health. Furthermore new aging models will be developed and better characterized for future aging and urological related research.
摘要

项目成果

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WILLIAM A RICKE其他文献

WILLIAM A RICKE的其他文献

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{{ truncateString('WILLIAM A RICKE', 18)}}的其他基金

Estrogen pathways in the development of prostatic fibrosis and lower urinary tract dysfunction
前列腺纤维化和下尿路功能障碍发展中的雌激素途径
  • 批准号:
    10378476
  • 财政年份:
    2021
  • 资助金额:
    $ 58.47万
  • 项目类别:
Estrogen pathways in the development of prostatic fibrosis and lower urinary tract dysfunction
前列腺纤维化和下尿路功能障碍发展中的雌激素途径
  • 批准号:
    10597683
  • 财政年份:
    2021
  • 资助金额:
    $ 58.47万
  • 项目类别:
Elucidating hallmarks of aging in the development of lower urinary tract dysfunction (LUTD)
阐明下尿路功能障碍 (LUTD) 发展中的衰老特征
  • 批准号:
    10346265
  • 财政年份:
    2021
  • 资助金额:
    $ 58.47万
  • 项目类别:
Elucidating hallmarks of aging in the development of lower urinary tract dysfunction (LUTD)
阐明下尿路功能障碍 (LUTD) 发展中的衰老特征
  • 批准号:
    10494151
  • 财政年份:
    2021
  • 资助金额:
    $ 58.47万
  • 项目类别:
Cellular and molecular mediators of fibrosis in the development of urinary tract dysfunction
尿路功能障碍发展过程中纤维化的细胞和分子介质
  • 批准号:
    9921105
  • 财政年份:
    2014
  • 资助金额:
    $ 58.47万
  • 项目类别:
Estrogens stimulate prostatic collagen synthesis to drive fibrosis and LUTD
雌激素刺激前列腺胶原蛋白合成,促进纤维化和 LUTD
  • 批准号:
    10700924
  • 财政年份:
    2014
  • 资助金额:
    $ 58.47万
  • 项目类别:
Estrogens stimulate prostatic collagen synthesis to drive fibrosis and LUTD
雌激素刺激前列腺胶原蛋白合成,促进纤维化和 LUTD
  • 批准号:
    10264805
  • 财政年份:
    2014
  • 资助金额:
    $ 58.47万
  • 项目类别:
Cellular and molecular mediators of fibrosis in the development of urinary tract dysfunction
尿路功能障碍发展过程中纤维化的细胞和分子介质
  • 批准号:
    10331481
  • 财政年份:
    2014
  • 资助金额:
    $ 58.47万
  • 项目类别:
Mediators of fibrosis in the development of lower urinary tract dysfunction
下尿路功能障碍发展中纤维化的介质
  • 批准号:
    9089461
  • 财政年份:
    2014
  • 资助金额:
    $ 58.47万
  • 项目类别:
Mediators of fibrosis in the development of lower urinary tract dysfunction
下尿路功能障碍发展中纤维化的介质
  • 批准号:
    9353662
  • 财政年份:
    2014
  • 资助金额:
    $ 58.47万
  • 项目类别:

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