Sirtuin-dependent metabolic and epigenetic regulation of macrophages during tuberculosis.
Sirtuin-dependent metabolic and epigenetic regulation of macrophages during tuberculosis.
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DOI：
10.3389/fimmu.2023.1121495
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发表时间：
2023
影响因子：
7.3
通讯作者：
中科院分区：
文献类型：
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作者：
巨噬细胞是控制多种感染的卓越吞噬细胞。结核病是人类死亡的主要原因，结核分枝杆菌（MTB）感染巨噬细胞并在巨噬细胞中存活。巨噬细胞利用活性氧和氮物质（ROS/RNS）和自噬来杀死和降解包括MTB在内的微生物。葡萄糖代谢调节巨噬细胞介导的抗菌机制。尽管葡萄糖对于免疫细胞中的细胞生长是必需的，但葡萄糖代谢及其下游代谢途径产生关键介体，其是组蛋白的翻译后修饰的必需共底物，组蛋白的翻译后修饰进而表观遗传地调节基因表达。在本文中，我们描述了sirtuins的作用，这是NAD+依赖性组蛋白/蛋白脱乙酰酶在自噬的表观遗传调控，ROS/RNS，乙酰辅酶A，NAD+，和S-腺苷蛋氨酸（SAM）的生产，并说明免疫代谢和表观遗传学之间的串扰对巨噬细胞活化。我们强调sirtuins作为新兴的治疗目标，修改免疫代谢，改变巨噬细胞表型和抗菌功能。
Macrophages are the preeminent phagocytic cells which control multiple infections. Tuberculosis a leading cause of death in mankind and the causative organism Mycobacterium tuberculosis (MTB) infects and persists in macrophages. Macrophages use reactive oxygen and nitrogen species (ROS/RNS) and autophagy to kill and degrade microbes including MTB. Glucose metabolism regulates the macrophage-mediated antimicrobial mechanisms. Whereas glucose is essential for the growth of cells in immune cells, glucose metabolism and its downsteam metabolic pathways generate key mediators which are essential co-substrates for post-translational modifications of histone proteins, which in turn, epigenetically regulate gene expression. Herein, we describe the role of sirtuins which are NAD+-dependent histone histone/protein deacetylases during the epigenetic regulation of autophagy, the production of ROS/RNS, acetyl-CoA, NAD+, and S-adenosine methionine (SAM), and illustrate the cross-talk between immunometabolism and epigenetics on macrophage activation. We highlight sirtuins as emerging therapeutic targets for modifying immunometabolism to alter macrophage phenotype and antimicrobial function.
影响因子：
5.6
作者：
Cahill C;Cox DJ;O'Connell F;Basdeo SA;Gogan KM;Ó'Maoldomhnaigh C;O'Sullivan J;Keane J;Phelan JJ
通讯作者：
Phelan JJ
影响因子：
3.7
作者：
Kim H;Shibayama K;Rimbara E;Mori S
通讯作者：
Mori S
影响因子：
--
作者：
Rahman A;Srivastava SS;Sneh A;Ahmed N;Krishnasastry MV
通讯作者：
Krishnasastry MV