It is our goal to better understand the molecular basis of structural and functional changes that occur in old kidneys during acute and chronic disease.
In studying these changes we put special emphasis on the tubulointerstitium, a compartment which comprises the bulk of the kidney. While the aging renal tubular system undergoes atrophy the interstitium increases in mass. This is associated with a progressive loss in renal function.
Similar changes can also occur in young patients and even in the pediatric population if the kidneys are challenged by noxious stressors that induce processes such accelerated aging and senescence.
We are interested in characterizing the underlying mechanisms of these changes in old and in stressed kidneys by applying different in vivo and in vitro models.