Nicotinamide adenine dinucleotide (NAD) has recently attracted much attention due to its role in aging and lifespan extension. NAD directly and indirectly affects many cellular processes, including metabolic pathways, DNA repair, and immune cell activities. These mechanisms are critical for maintaining cellular homeostasis. However, the decline in NAD levels with aging impairs tissue function, which has been associated with several age-related diseases. In fact, the aging population has been steadily increasing worldwide, and it is important to restore NAD levels and reverse or delay these age-related disorders. Therefore, there is an increasing demand for healthy products that can mitigate aging, extend lifespan, and halt age-related consequences. In this case, several studies in humans and animals have targeted NAD metabolism with NAD intermediates. Among them, nicotinamide mononucleotide (NMN), a precursor in the biosynthesis of NAD, has recently received much attention from the scientific community for its anti-aging properties. In model organisms, ingestion of NMN has been shown to improve age-related diseases and probably delay death. Here, we review aspects of NMN biosynthesis and the mechanism of its absorption, as well as potential anti-aging mechanisms of NMN, including recent preclinical and clinical tests, adverse effects, limitations, and perceived challenges.
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http://dx.doi.org/10.14336/AD.2023.0519-1 | DOI Listing |
J Inflamm Res
January 2025
State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, People's Republic of China.
Purpose: Oral lichen planus (OLP) is a chronic, immune-mediated inflammatory disease involving T cells. Mitochondrial fission plays a crucial role in T cell fate through structural remodeling. Nicotinamide adenine dinucleotide (NAD) regulates mitochondrial remodeling and function.
View Article and Find Full Text PDFNPJ Aging
January 2025
Department of Developmental Biology, Department of Medicine (Joint), Washington University School of Medicine, St. Louis, Missouri, USA.
Over the past five years, systemic NAD (nicotinamide adenine dinucleotide) decline has been accepted to be a key driving force of aging in the field of aging research. The original version of the NAD World concept was proposed in 2009, providing an integrated view of the NAD-centric, systemic regulatory network for mammalian aging and longevity control. The reformulated version of the concept, the NAD World 2.
View Article and Find Full Text PDFiScience
January 2025
Department of Vascular Surgery, Lausanne University Hospital (CHUV), Lausanne, Switzerland.
Aging is accompanied by a decline in neovascularization potential and increased susceptibility to ischemic injury. Here, we confirm the age-related impaired neovascularization following ischemic leg injury and impaired angiogenesis. The age-related deficits in angiogenesis arose primarily from diminished EC proliferation capacity, but not migration or VEGF sensitivity.
View Article and Find Full Text PDFBiotechnol Appl Biochem
January 2025
Department of Chemical Engineering, Chungbuk National University, Cheongju, Chungbuk, Republic of Korea.
The PnuC gene plays a crucial role in the complex processes related to the absorption and synthesis of the nicotinamide mononucleotide (NMN) precursor. NMN, a nicotinamide adenine dinucleotide (NAD) precursor, is important for cellular energy metabolism, DNA repair, and antiaging. This study focuses on elucidating the precursor absorption mechanism and the specific function of the PnuC gene in encoding membrane transport proteins, as well as its impact on the regulation and dynamics of NMN within the cell.
View Article and Find Full Text PDFLupus Sci Med
January 2025
Dermatology, The University of Texas Southwestern Medical Center, Dallas, Texas, USA
Objective: Metabolic reprogramming plays a critical role in modulating the innate and adaptive immune response, but its role in cutaneous autoimmune diseases, such as cutaneous lupus erythematosus (CLE), is less well studied. An improved understanding of the metabolic pathways dysregulated in CLE may lead to novel treatment options, biomarkers and insights into disease pathogenesis. The objective was to compare metabolomic profiles in the skin and sera of CLE and control patients using liquid chromatography-mass spectrometry (LC-MS).
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