NAD+ enhancers as therapeutic agents in the cardiorenal axis
Cardiorenal diseases represent a complex interplay between heart failure and renal dysfunction, being clinically classified as cardiorenal syndromes (CRS). Recently, the contributions of altered nicotinamide adenine dinu-cleotide (NAD+) metabolism, through deficient NAD+ synthesis and/or elevated co...
| Autores: | , , , , |
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| Tipo de recurso: | artículo |
| Fecha de publicación: | 2024 |
| País: | España |
| Institución: | Universidad Católica San Antonio de Murcia (UCAM) |
| Repositorio: | RIUCAM. Repositorio Institucional de la Universidad Católica San Antonio de Murcia |
| OAI Identifier: | oai:repositorio.ucam.edu:10952/8905 |
| Acceso en línea: | http://hdl.handle.net/10952/8905 |
| Access Level: | acceso abierto |
| Palabra clave: | Cardiorenal syndrome NAD+ metabolism Niacin Nicotinamide Nicotinamide riboside Nicotinamide mononucleotide Poly(ADP-ribose) polymerases Sirtuins CD38 NRH NMNH Trigonelline Ischemia/reperfusion AKI Animal models Clinical trials |
| Sumario: | Cardiorenal diseases represent a complex interplay between heart failure and renal dysfunction, being clinically classified as cardiorenal syndromes (CRS). Recently, the contributions of altered nicotinamide adenine dinu-cleotide (NAD+) metabolism, through deficient NAD+ synthesis and/or elevated consumption, have proved to be decisive in the onset and progress of cardiorenal disease. NAD+ is a pivotal coenzyme in cellular metabolism, being significant in various signaling pathways, such as energy metabolism, DNA damage repair, gene ex-pression, and stress response. Convincing evidence suggests that strategies designed to boost cellular NAD+ levels are a promising therapeutic option to address cardiovascular and renal disorders. Here, we review and discuss the implications of NAD+ metabolism in cardiorenal diseases, focusing on the propitious NAD+ boosting therapeutic strategies, based on the use of NAD+ precursors, poly(ADP-ribose) polymerase inhibitors, sirtuin activators, and other alternative approaches, such as CD38 blockade, nicotinamide phosphoribosyltransferase activation and combined interventions. |
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