Abstract
Aging in most species is associated with impaired adaptive and homeostatic mechanisms, leading to susceptibility to environmental or internal stresses with increasing rates of disease. A number of different theories of primarily disease-independent renal aging, which can be categorized as evolutionary, molecular, cellular and systemic, have been put forward in the past decades, and recent studies have provided evidence for some of them. This review is focused on the several mechanisms that are considered to underlie the primary aging process and contribute to age-related changes and adaptive responses in the kidney. These mechanisms include genetic modulations, telomere shortening, oxidative stress and mitochondrial dysfunction, all markers of cell senescence. Moreover, we also highlight new advances in understanding functions of angiotensin II type 1 (AT1) receptor that contribute to the renal aging process. Here we review recent advances in understanding the role of Klotho, sirtuins, cell senescence through oxidative stress and mitochondrial dysfunction, as well as of the renin-angiotensin system in modulating age-related kidney damage.
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