NAD+激酶
烟酰胺腺嘌呤二核苷酸
辅因子
生物合成
烟酰胺
肾脏疾病
急性肾损伤
医学
生物化学
化学
生物
酶
内科学
作者
Amanda J. Clark,Marie Christelle Saade,Samir M. Parikh
标识
DOI:10.1016/j.semnephrol.2022.10.013
摘要
Acute kidney injury (AKI) is a serious and highly prevalent disease, yet only supportive treatment is available. Nicotinamide adenine dinucleotide (NAD+) is a cofactor necessary for adenosine triphosphate (ATP) production and cell survival. Changes in renal NAD+ biosynthesis and energy utilization are features of AKI. Targeting NAD+ as an AKI therapy shows promising potential. However, the pursuit of NAD+-based treatments requires deeper understanding of the unique drivers and effects of the NAD+ biosynthesis derangements that arise in AKI. This article summarizes the NAD+ biosynthesis alterations in the kidney in AKI, chronic disease, and aging. To enhance this understanding, we explore instances of NAD+ biosynthesis alterations outside the kidney in inflammation, pregnancy, and cancer. In doing so, we seek to highlight that the different NAD+ biosynthesis pathways are not interconvertible and propose that the way in which NAD+ is synthesized may be just as important as the NAD+ produced.
科研通智能强力驱动
Strongly Powered by AbleSci AI