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. Despite the crucial importance of the kidney both as a prime target and most likely determinant of human aging, knowledge of the mechanisms underlying age-associated kidney damage is very limited. While certain parts of the kidney are continuously replaced, allowing for constant regeneration, some highly differentiated kidney cells like podocytes fulfill specialized tasks and cannot be easily exchanged. We have recently identified the mTOR-autophagy axis as critical determinant of glomerular aging and have set up a complementary set of mouse models to study the precise molecular events regulating kidney aging. In addition, our laboratory coordinates and is part of the multidsiciplinary  BMBF funded programm -NephAge-, which is establishing a multi-organism, multi-timescale, systems biology approach that allows for the combined measurement, analysis and modeling of the global and dynamic alterations in aging kidney tissue.