促炎细胞因子
败血症
铁蛋白
表型
髓样
炎症
髓系细胞
免疫学
生物
医学
遗传学
基因
内科学
作者
James D. Odum,Juheb Akhter,Vivek Verma,Giacynta A. Vollmer,Ahmad Davidson,Kelly A. Hyndman,Subhashini Bolisetty
出处
期刊:American Journal of Physiology-renal Physiology
[American Physical Society]
日期:2024-05-23
卷期号:327 (1): F171-F183
被引量:8
标识
DOI:10.1152/ajprenal.00043.2024
摘要
Hyperferritinemia in sepsis is often associated with a proinflammatory phenotype and poor prognosis. We previously showed the myeloid deletion of FtH results in a compensatory increase in FtL and is associated with reduced circulating cytokines and decreased rates of SA-AKI in animal sepsis models. Here, we show that myeloid deletion of FtL does not impact the severity of SA-AKI following CLP or LPS, suggesting that FtH plays the predominant role in propagating myeloid-induced proinflammatory pathways.
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