糖酵解
重编程
细胞生物学
生物
哮喘
巨噬细胞
癌症研究
化学
炎症
新陈代谢
免疫学
转录组
厌氧糖酵解
中性粒细胞
下调和上调
脂质代谢
髓系细胞
趋化性
生物化学
医学
疾病
代谢途径
作者
Guomei Su,Jiangyun Peng,Jieru Quan,Zhihang Feng,Yu Zhong,Zhilin Xiong,Jiewen Huang,Zhao Zhao,Yingying Lv,Wenhong Hou,Lianxiang Luo,Xiao Li,Yiming Shao,Jielin Duan,Xiao Gao,Tianwen Lai
出处
期刊:Cell Reports
[Cell Press]
日期:2026-04-21
卷期号:45 (5): 117294-117294
被引量:1
标识
DOI:10.1016/j.celrep.2026.117294
摘要
-dependent deacetylase Sirtuin 6 (SIRT6) regulates immune responses, its role in neutrophilic asthma remains unknown. Utilizing multiple human samples and neutrophilic asthma murine model, we identify macrophage SIRT6 as a key regulator that governs airway neutrophil infiltration in severe asthma. Myeloid-specific Sirt6 deletion attenuates allergen-induced airway neutrophil infiltration by suppressing lactate dehydrogenase A (LDHA)-mediated lactate production and neutrophil-recruiting chemokines secretion. Mechanistically, SIRT6 directly interacts with LDHA and deacetylates LDHA at lysine 261 (K261) via SIRT6-N-terminal domain. Lactate accumulation promotes histone H4 lysine 12 (H4K12) lactylation, up-regulating Cxcl1 and Cxcl2 transcription to drive airway neutrophil infiltration. Importantly, we screen flavonoid astragalin as a specific SIRT6 inhibitor that attenuates airway neutrophil infiltration in severe asthmatic mice. Collectively, our findings reveal a critical role of the SIRT6-mediated metabolic reprogramming in neutrophilic asthma and establish SIRT6 as a promising therapeutic target.
科研通智能强力驱动
Strongly Powered by AbleSci AI