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NAD+ and Vascular Dysfunction: From Mechanisms to Therapeutic Opportunities.


ABSTRACT: Nicotinamide adenine dinucleotide (NAD+) is an essential and pleiotropic coenzyme involved not only in cellular energy metabolism, but also in cell signaling, epigenetic regulation, and post-translational protein modifications. Vascular disease risk factors are associated with aberrant NAD+ metabolism. Conversely, the therapeutic increase of NAD+ levels through the administration of NAD+ precursors or inhibitors of NAD+-consuming enzymes reduces chronic low-grade inflammation, reactivates autophagy and mitochondrial biogenesis, and enhances oxidative metabolism in vascular cells of humans and rodents with vascular pathologies. As such, NAD+ has emerged as a potential target for combatting age-related cardiovascular and cerebrovascular disorders. This review discusses NAD+-regulated mechanisms critical for vascular health and summarizes new advances in NAD+ research directly related to vascular aging and disease, including hypertension, atherosclerosis, coronary artery disease, and aortic aneurysms. Finally, we enumerate challenges and opportunities for NAD+ repletion therapy while anticipating the future of this exciting research field, which will have a major impact on vascular medicine.

SUBMITTER: Abdellatif M 

PROVIDER: S-EPMC9133775 | biostudies-literature | 2022 May

REPOSITORIES: biostudies-literature

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NAD<sup>+</sup> and Vascular Dysfunction: From Mechanisms to Therapeutic Opportunities.

Abdellatif Mahmoud M   Bugger Heiko H   Kroemer Guido G   Sedej Simon S  

Journal of lipid and atherosclerosis 20220406 2


Nicotinamide adenine dinucleotide (NAD<sup>+</sup>) is an essential and pleiotropic coenzyme involved not only in cellular energy metabolism, but also in cell signaling, epigenetic regulation, and post-translational protein modifications. Vascular disease risk factors are associated with aberrant NAD<sup>+</sup> metabolism. Conversely, the therapeutic increase of NAD<sup>+</sup> levels through the administration of NAD<sup>+</sup> precursors or inhibitors of NAD<sup>+</sup>-consuming enzymes red  ...[more]

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