溃疡性结肠炎
NAD+激酶
肿瘤坏死因子α
肠道菌群
结肠炎
化学
微生物学
医学
药理学
免疫学
生物化学
生物
内科学
酶
疾病
作者
Lei Jing,Lin Lv,Li Zhong,Feng Xu,Wen‐Hao Su,Yan Chen,Yan Chen,Zhixuan Wu,Song He,Yongyu Chen,Yongyu Chen
出处
期刊:Advanced Science
[Wiley]
日期:2024-12-30
卷期号:12 (8): e2413128-e2413128
被引量:14
标识
DOI:10.1002/advs.202413128
摘要
) salvage pathway by upregulating NAMPT expression, which subsequently leads to the activation of the p38 mitogen-activated protein kinase (MAPK) signaling pathway and promotes the secretion of inflammatory factors, ultimately inhibiting the therapeutic response to anti-TNF drugs. These findings demonstrate that the gut microbiota can influence the response to anti-TNF therapy in patients with UC and highlight the therapeutic potential of targeting F. nucleatum and its associated pathways for preventing and treating drug resistance in UC.
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