
Dysregulation of the NAD Metabolome in Acute Kidney Injury
Aging is a naturally occurring phenomenon that is accelerated by different diseases and stressors. The importance of this area is significant, as the world population grows older due to decreasing mortality rates. In order to combat this issue, we are investigating an essential co-enzyme found in all living cells called Nicotinamide Adenine Dinucleotide (NAD+). Many think about NAD+ in the context of staple pathways such as glycolysis or the TCA cycle, but it has a much broader impact on metabolism and energy production. NAD+ decline has been implicated in advanced aging and disease, and often we see an overactivation of NAD+ consuming enzymes. One of the stressors associated with NAD+ decline is Acute Kidney Injury, a disease for which older individuals are more susceptible. The overarching goal of this project is to determine the driver of NAD+ decline amidst Acute Kidney Injury; is this decline more of a result of impaired synthesis or accelerated consumption? To investigate this question, we have established a cisplatin-induced Acute Kidney Injury murine model and analyzed circulating, tissue, and excretory metabolites via Liquid Chromatography-Coupled Mass Spectrometry. Steady state measurements can show important indicative trends, but alone they are insufficient to answer our questions. As a result, we have undergone preliminary stable isotope tracing experiments with plans to calculate the metabolic flux of NAD+ and define the nature of its decline in cases of kidney injury.
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Work Title | Dysregulation of the NAD Metabolome in Acute Kidney Injury |
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License | CC BY-SA 4.0 (Attribution-ShareAlike) |
Work Type | Research Paper |
Publication Date | April 26, 2024 |
Deposited | April 26, 2024 |
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