Akash Chakraborty1,2, Keaton E Minor1,3, Hina Lateef Nizami1, Ying Ann Chiao2,4, Chi Fung Lee5,6. 1. Cardiovascular Biology Research Program, MS 45, Oklahoma Medical Research Foundation, 825 NE 13th Street, Oklahoma City, OK, 73104, USA. 2. Aging and Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, USA. 3. Department of Physiology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA. 4. Department of Biochemistry and Molecular Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA. 5. Cardiovascular Biology Research Program, MS 45, Oklahoma Medical Research Foundation, 825 NE 13th Street, Oklahoma City, OK, 73104, USA. chifung-lee@omrf.org. 6. Department of Physiology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA. chifung-lee@omrf.org.
Abstract
PURPOSE OF THE REVIEW: This review summarizes current understanding on the roles of nicotinamide adenine dinucleotide (NAD+) metabolism in the pathogeneses and treatment development of metabolic and cardiac diseases. RECENT FINDINGS: NAD+ was identified as a redox cofactor in metabolism and a co-substrate for a wide range of NAD+-dependent enzymes. NAD+ redox imbalance and depletion are associated with many pathologies where metabolism plays a key role, for example cardiometabolic diseases. This review is to delineate the current knowledge about harnessing NAD+ metabolism as potential therapy for cardiometabolic diseases. The review has summarized how NAD+ redox imbalance and depletion contribute to the pathogeneses of cardiometabolic diseases. Therapeutic evidence involving activation of NAD+ synthesis in pre-clinical and clinical studies was discussed. While activation of NAD+ synthesis shows great promise for therapy, the field of NAD+ metabolism is rapidly evolving. Therefore, it is expected that new mechanisms will be discovered as therapeutic targets for cardiometabolic diseases.
PURPOSE OF THE REVIEW: This review summarizes current understanding on the roles of nicotinamide adenine dinucleotide (NAD+) metabolism in the pathogeneses and treatment development of metabolic and cardiac diseases. RECENT FINDINGS: NAD+ was identified as a redox cofactor in metabolism and a co-substrate for a wide range of NAD+-dependent enzymes. NAD+ redox imbalance and depletion are associated with many pathologies where metabolism plays a key role, for example cardiometabolic diseases. This review is to delineate the current knowledge about harnessing NAD+ metabolism as potential therapy for cardiometabolic diseases. The review has summarized how NAD+ redox imbalance and depletion contribute to the pathogeneses of cardiometabolic diseases. Therapeutic evidence involving activation of NAD+ synthesis in pre-clinical and clinical studies was discussed. While activation of NAD+ synthesis shows great promise for therapy, the field of NAD+ metabolism is rapidly evolving. Therefore, it is expected that new mechanisms will be discovered as therapeutic targets for cardiometabolic diseases.
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