Weir Heather J M, Lane Jon D, Balthasar Nina
School of Physiology and Pharmacology, University of Bristol, Bristol, UK.
Genes Cancer. 2013 Mar;4(3-4):118-24. doi: 10.1177/1947601913476949.
SIRT3 is a NAD(+)-dependent deacetylase that regulates the function of numerous mitochondrial proteins with roles in metabolism, oxidative stress, and cell survival. It is emerging as an instrumental regulator of the mitochondrial adaptive responses to stress, including metabolic reprogramming and enhancing antioxidant defense mechanisms. Here, we discuss the role that SIRT3 plays at both a cellular and physiological level and consider its involvement in disease. Mitochondrial dysfunction is a key contributing factor in many diseases; however, the mechanisms involved are often not well understood, and few targeted therapies exist. If manipulation of SIRT3 proves to be beneficial in disease states, then it could be a promising target for novel therapies.
SIRT3是一种依赖烟酰胺腺嘌呤二核苷酸（NAD(+)）的脱乙酰酶，可调节众多线粒体蛋白的功能，这些蛋白在代谢、氧化应激和细胞存活中发挥作用。它正逐渐成为线粒体应激适应性反应的重要调节因子，包括代谢重编程和增强抗氧化防御机制。在此，我们讨论SIRT3在细胞和生理水平上所起的作用，并探讨其与疾病的关联。线粒体功能障碍是许多疾病的关键促成因素；然而，其中涉及的机制往往尚未完全明确，且针对性治疗方法很少。如果证明操纵SIRT3对疾病状态有益，那么它可能成为新型治疗方法的一个有前景的靶点。
