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Boosting NAD+ blunts TLR4-induced type I IFN in control and systemic lupus erythematosus monocytes
The Journal of Clinical Investigation ( IF 15.9 ) Pub Date : 2022 , DOI: 10.1172/jci139828 Jing Wu 1 , Komudi Singh 1, 2 , Amy Lin 1 , Allison M Meadows 1 , Kaiyuan Wu 1 , Vivian Shing 1 , Maximilian Bley 1 , Shahin Hassanzadeh 1 , Rebecca D Huffstutler 3 , Mark S Schmidt 4 , Luz P Blanco 5 , Rong Tian 6 , Charles Brenner 4, 7 , Mehdi Pirooznia 2 , Mariana J Kaplan 5 , Michael N Sack 1, 3
The Journal of Clinical Investigation ( IF 15.9 ) Pub Date : 2022 , DOI: 10.1172/jci139828 Jing Wu 1 , Komudi Singh 1, 2 , Amy Lin 1 , Allison M Meadows 1 , Kaiyuan Wu 1 , Vivian Shing 1 , Maximilian Bley 1 , Shahin Hassanzadeh 1 , Rebecca D Huffstutler 3 , Mark S Schmidt 4 , Luz P Blanco 5 , Rong Tian 6 , Charles Brenner 4, 7 , Mehdi Pirooznia 2 , Mariana J Kaplan 5 , Michael N Sack 1, 3
Affiliation
BACKGROUND. Fasting and NAD+-boosting compounds, including NAD+ precursor nicotinamide riboside (NR), confer antiinflammatory effects. However, the underlying mechanisms and therapeutic potential are incompletely defined.
中文翻译：
在对照和系统性红斑狼疮单核细胞中增强 NAD+ 可减弱 TLR4 诱导的 I 型干扰素
背景。禁食和促进 NAD +的化合物，包括 NAD +前体烟酰胺核苷 (NR)，具有抗炎作用。然而，潜在的机制和治疗潜力尚未完全确定。
更新日期：2022-03-01
中文翻译：
在对照和系统性红斑狼疮单核细胞中增强 NAD+ 可减弱 TLR4 诱导的 I 型干扰素
背景。禁食和促进 NAD +的化合物，包括 NAD +前体烟酰胺核苷 (NR)，具有抗炎作用。然而，潜在的机制和治疗潜力尚未完全确定。
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