Roles of NAD + in Acute and Chronic Kidney Diseases.

Autor: Morevati M; Department of Nephrology, Rigshospitalet, University of Copenhagen, 2100 Copenhagen, Denmark., Fang EF; Department of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, 1478 Lørenskog, Norway., Mace ML; Department of Nephrology, Rigshospitalet, University of Copenhagen, 2100 Copenhagen, Denmark., Kanbay M; Division of Nephrology, Department of Medicine, Koç University School of Medicine, Istanbul 34010, Turkey., Gravesen E; Department of Pathology, Herlev Hospital, University of Copenhagen, 2730 Copenhagen, Denmark., Nordholm A; Department of Nephrology, Rigshospitalet, University of Copenhagen, 2100 Copenhagen, Denmark., Egstrand S; Department of Nephrology, Rigshospitalet, University of Copenhagen, 2100 Copenhagen, Denmark., Hornum M; Department of Nephrology, Rigshospitalet, University of Copenhagen, 2100 Copenhagen, Denmark.
Jazyk: angličtina
Zdroj: International journal of molecular sciences [Int J Mol Sci] 2022 Dec 21; Vol. 24 (1). Date of Electronic Publication: 2022 Dec 21.
DOI: 10.3390/ijms24010137
Abstrakt: Nicotinamide adenine dinucleotide (oxidized form, NAD + ) is a critical coenzyme, with functions ranging from redox reactions and energy metabolism in mitochondrial respiration and oxidative phosphorylation to being a central player in multiple cellular signaling pathways, organ resilience, health, and longevity. Many of its cellular functions are executed via serving as a co-substrate for sirtuins (SIRTs), poly (ADP-ribose) polymerases (PARPs), and CD38. Kidney damage and diseases are common in the general population, especially in elderly persons and diabetic patients. While NAD + is reduced in acute kidney injury (AKI) and chronic kidney disease (CKD), mounting evidence indicates that NAD + augmentation is beneficial to AKI, although conflicting results exist for cases of CKD. Here, we review recent progress in the field of NAD + , mainly focusing on compromised NAD + levels in AKI and its effect on essential cellular pathways, such as mitochondrial dysfunction, compromised autophagy, and low expression of the aging biomarker αKlotho (Klotho) in the kidney. We also review the compromised NAD + levels in renal fibrosis and senescence cells in the case of CKD. As there is an urgent need for more effective treatments for patients with injured kidneys, further studies on NAD + in relation to AKI/CKD may shed light on novel therapeutics.
Databáze: MEDLINE
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