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About the Authors:
María José Hernández-Corbacho
Affiliation: Department of Medicine Medical University of South Carolina, Charleston, South Carolina, United States of America
Russell W. Jenkins
Affiliation: Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, South Carolina, United States of America
Christopher J. Clarke
Affiliation: Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, South Carolina, United States of America
Yusuf A. Hannun
Affiliation: Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, South Carolina, United States of America
Lina M. Obeid
Affiliations Department of Medicine Medical University of South Carolina, Charleston, South Carolina, United States of America, Ralph H. Johnson Veterans Affairs Medical Center, Charleston, South Carolina, United States of America
Ashley J. Snider
Affiliations Department of Medicine Medical University of South Carolina, Charleston, South Carolina, United States of America, Ralph H. Johnson Veterans Affairs Medical Center, Charleston, South Carolina, United States of America
Leah J. Siskind
* E-mail: [email protected]
Affiliations Department of Medicine Medical University of South Carolina, Charleston, South Carolina, United States of America, Ralph H. Johnson Veterans Affairs Medical Center, Charleston, South Carolina, United States of America
Introduction
Many factors are thought to contribute to mammalian aging including changes in gene expression, mitochondrial dysfunction, oxidative stress, shortening of telomeres, and accumulation of advanced glycation end-products. These factors eventually lead to a decline in organ function and the ability to respond to physiological and pathophysiological stimuli. In the kidney, there is an age-associated progressive deterioration in renal function even in the absence of obvious renal disease [1]–[3]. Moreover, many changes occur in the kidney prior to a decline in kidney function, including increases in pro-inflammatory enzymes and cytokines [4], [5]. Consequently, elucidating the early changes that lead to a decline in kidney function is critical for the development of therapeutics aimed at preserving kidney function during aging.
With normal aging, a number of functional and structural changes occur in the kidney both in humans and in laboratory animals. These include decreases in renal blood flow and glomerular filtration rate, changes in tubular function that impair the ability to concentrate urine, glomerulosclerosis, and tubulointerstitial fibrosis [1]–[3]. Furthermore, as drug excretion is also reduced in the aged kidney, the pharmacokinetics and pharmacodynamics of many drugs...