Abstract
Pedigree genetics and environment modulate the biological process of aging. The permanent and irreversible growth arrest of cell senescence is a central paradigm of aging. Various pathophysiologic pressures such as oxidative stress and mitochondrial injury can also induce senescence. Senescent cells secrete altered levels of growth factors, show increased susceptibility to apoptosis, and associate with delayed repair and regeneration in the aging kidney. Here we discuss new progress in understanding renal aging, focusing on mechanisms of cell senescence and possible interventions to modulate age-related organ damage.
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