The kidney is susceptible to age-dependent alterations in structure that lead to renal dysfunction, including an increased susceptibility to acute kidney injury (AKI). Our laboratory is focused on projects investigating the increased susceptibility of the aging kidney to injury in hopes of developing prevention and treatment strategies to manage the increasing burden of renal disease in the geriatric population.

Project 1

We have identified an age-related loss of N-cadherin in the kidney (Jung et al., 2004; Akintola et al., 2008). Current work is focused on the role of N-cadherin loss in the development of tubulointerstitial fibrosis via epithelial-to-mesenchymal transition (EMT) of proximal tubular epithelial cells.

Project 2

The expression and activity of several MMPs is increased in the aging kidney (Chen et al., 2007b) and have also identified cadherins as important MMP substrates in renal ischemia-reperfusion injury (Covington et al., 2005; Covington et al., 2006). We are focusing on the role of MMPs in acute kidney injury, specifically the relationship between MMP-mediated cadherin cleavage and the initiation of acute kidney injury.