Alhumaidi Rahil, Huang Huihui, Saade Marie Christelle, Clark Amanda J, Parikh Samir M
Division of Nephrology, Department of Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Division of Nephrology, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, MA, USA.
Trends Mol Med. 2025 Jul;31(7):669-681. doi: 10.1016/j.molmed.2024.12.004. Epub 2025 Jan 4.
Disturbances in kidney tubular cell metabolism are increasingly recognized as a feature of acute kidney injury (AKI). In AKI, tubular epithelial cells undergo abnormal metabolic shifts that notably disrupt NAD metabolism. Recent advancements have highlighted the critical role of NAD metabolism in AKI, revealing that acute disruptions may lead to lasting cellular changes, thereby promoting the transition to chronic kidney disease (CKD). This review explores the molecular mechanisms underlying metabolic dysfunction in AKI, with a focus on NAD metabolism, and proposes several cellular processes through which acute aberrations in NAD may contribute to long-term changes in the kidney.
肾小管细胞代谢紊乱日益被认为是急性肾损伤(AKI)的一个特征。在急性肾损伤中,肾小管上皮细胞会发生异常的代谢转变,显著扰乱NAD代谢。最近的进展突出了NAD代谢在急性肾损伤中的关键作用,表明急性干扰可能导致持久的细胞变化,从而促进向慢性肾病(CKD)的转变。本综述探讨了急性肾损伤中代谢功能障碍的分子机制,重点关注NAD代谢,并提出了NAD急性异常可能导致肾脏长期变化的几种细胞过程。