Roles of NAD<sup>+</sup> in Acute and Chronic Kidney Diseases
Nicotinamide adenine dinucleotide (oxidized form, NAD<sup>+</sup>) 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...
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MDPI AG
2022-12-01
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Online Access: | https://www.mdpi.com/1422-0067/24/1/137 |
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author | Marya Morevati Evandro Fei Fang Maria L. Mace Mehmet Kanbay Eva Gravesen Anders Nordholm Søren Egstrand Mads Hornum |
author_facet | Marya Morevati Evandro Fei Fang Maria L. Mace Mehmet Kanbay Eva Gravesen Anders Nordholm Søren Egstrand Mads Hornum |
author_sort | Marya Morevati |
collection | DOAJ |
description | Nicotinamide adenine dinucleotide (oxidized form, NAD<sup>+</sup>) 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<sup>+</sup> is reduced in acute kidney injury (AKI) and chronic kidney disease (CKD), mounting evidence indicates that NAD<sup>+</sup> augmentation is beneficial to AKI, although conflicting results exist for cases of CKD. Here, we review recent progress in the field of NAD<sup>+</sup>, mainly focusing on compromised NAD<sup>+</sup> 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<sup>+</sup> 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<sup>+</sup> in relation to AKI/CKD may shed light on novel therapeutics. |
first_indexed | 2024-03-11T10:00:23Z |
format | Article |
id | doaj.art-eb8bcb81d0564ca0ae4e8a74793de37b |
institution | Directory Open Access Journal |
issn | 1661-6596 1422-0067 |
language | English |
last_indexed | 2024-03-11T10:00:23Z |
publishDate | 2022-12-01 |
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record_format | Article |
series | International Journal of Molecular Sciences |
spelling | doaj.art-eb8bcb81d0564ca0ae4e8a74793de37b2023-11-16T15:29:56ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672022-12-0124113710.3390/ijms24010137Roles of NAD<sup>+</sup> in Acute and Chronic Kidney DiseasesMarya Morevati0Evandro Fei Fang1Maria L. Mace2Mehmet Kanbay3Eva Gravesen4Anders Nordholm5Søren Egstrand6Mads Hornum7Department of Nephrology, Rigshospitalet, University of Copenhagen, 2100 Copenhagen, DenmarkDepartment of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, 1478 Lørenskog, NorwayDepartment of Nephrology, Rigshospitalet, University of Copenhagen, 2100 Copenhagen, DenmarkDivision of Nephrology, Department of Medicine, Koç University School of Medicine, Istanbul 34010, TurkeyDepartment of Pathology, Herlev Hospital, University of Copenhagen, 2730 Copenhagen, DenmarkDepartment of Nephrology, Rigshospitalet, University of Copenhagen, 2100 Copenhagen, DenmarkDepartment of Nephrology, Rigshospitalet, University of Copenhagen, 2100 Copenhagen, DenmarkDepartment of Nephrology, Rigshospitalet, University of Copenhagen, 2100 Copenhagen, DenmarkNicotinamide adenine dinucleotide (oxidized form, NAD<sup>+</sup>) 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<sup>+</sup> is reduced in acute kidney injury (AKI) and chronic kidney disease (CKD), mounting evidence indicates that NAD<sup>+</sup> augmentation is beneficial to AKI, although conflicting results exist for cases of CKD. Here, we review recent progress in the field of NAD<sup>+</sup>, mainly focusing on compromised NAD<sup>+</sup> 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<sup>+</sup> 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<sup>+</sup> in relation to AKI/CKD may shed light on novel therapeutics.https://www.mdpi.com/1422-0067/24/1/137NAD<sup>+</sup>mitochondriaautophagyacute kidney injuryKlothochronic kidney disease |
spellingShingle | Marya Morevati Evandro Fei Fang Maria L. Mace Mehmet Kanbay Eva Gravesen Anders Nordholm Søren Egstrand Mads Hornum Roles of NAD<sup>+</sup> in Acute and Chronic Kidney Diseases International Journal of Molecular Sciences NAD<sup>+</sup> mitochondria autophagy acute kidney injury Klotho chronic kidney disease |
title | Roles of NAD<sup>+</sup> in Acute and Chronic Kidney Diseases |
title_full | Roles of NAD<sup>+</sup> in Acute and Chronic Kidney Diseases |
title_fullStr | Roles of NAD<sup>+</sup> in Acute and Chronic Kidney Diseases |
title_full_unstemmed | Roles of NAD<sup>+</sup> in Acute and Chronic Kidney Diseases |
title_short | Roles of NAD<sup>+</sup> in Acute and Chronic Kidney Diseases |
title_sort | roles of nad sup sup in acute and chronic kidney diseases |
topic | NAD<sup>+</sup> mitochondria autophagy acute kidney injury Klotho chronic kidney disease |
url | https://www.mdpi.com/1422-0067/24/1/137 |
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