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Research Programme

Background

 

The aging process leads to a progressive deterioration of tissues and organs, resulting in impaired tissue function, increased organismal vulnerability, and death. Improving health in the elderly will be crucial to deal with the enormous socio-economic challenges arising as a consequence of increased life expectancy. Aging is the driving force for the most prevalent chronic diseases, including coronary heart and kidney disease. Interestingly, the kidney represents a prime target of age-associated organ damage, which is reflected by the clear association of renal function decline with age. Chronic kidney diseases (CKD) are of high public health importance not only because of their high prevalence among the elderly, but also because they are a major independent risk factor for cardiovascular morbidity and mortality. Despite the crucial importance of the kidney both as a prime target and most likely determinant of human aging (Khan et al, Kidney Int, 2002; Sarnak et al, Circulation 2003), knowledge of the mechanisms underlying age-associated kidney damage is very limited. Studies designed to determine such molecular mechanisms will help formulate therapeutic interventions that delay the onset and/or progression of CKD in elderly patients.

 

Approach

 

The approaches which we will take to understand the aging process of the kidney are through:

  1. Monitoring of proteomic, transcriptomic and metabolomic data from mouse models across various cellular determinants and parameters.
  2. Genes identified in GWAS of kidney disease in elderly individuals will be subjected to screens for genes, compounds, and kinases putatively modulating age-related phenotypes in C.elegans and D. melanogaster.
  3. Based on high throughput data from aims 1 and 2, a systemic characterization relating kidney age to cell status will be developed, relating ‘omics’, characteristics to phenotype.
  4. In order to develop intervention strategies alleviating cell function deficiencies, an iterative systems biology modeling cycle will be established, elucidating in vitro- and in vivo dynamic effects of aging on signaling pathways and cellular decisions on time scales of minutes to days.
  5. The above steps enable us to rapidly test hypotheses in silico for their in vivo-relevance in our model organisms via standard molecular tools and for their clinical relevance in human cohort studies.

 

Aims

 

The common goals of the scientists jointly working in the NephAge consortium are:

  1. Identification of fundamental biological mechanisms of aging in the kidney, which may ultimately aid in risk prediction and improved targeted medical interventions to promote healthy aging in general.
  2. Identification of predictive kidney aging biomarkers and target candidates for therapeutic intervention.
  3. Assessment of personalized age progression and relative risk potential for age-related (chronic kidney disease).
  4. Development of simple tests that determine a ‘personalized age’, which will be of substantial economic interest (in cooperation with our industrial partners).
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