13 Papers
29 Citations
Fei Tu is an academic researcher from East Tennessee State University James H. Quillen College of Medicine. The author has contributed to research in topics: Sepsis & Medicine. The author has an hindex of 7, co-authored 9 publications. Previous affiliations of Fei Tu include East Tennessee State University & Tennessee State University.
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Papers
Lactate promotes macrophage HMGB1 lactylation, acetylation, and exosomal release in polymicrobial sepsis.
Kun Yang,Kun Yang,Min Fan,Min Fan,Xiaohui Wang,Xiaohui Wang,Jingjing Xu,Yana Wang,Fei Tu,P. Spencer Gill,Tuanzhu Ha,Tuanzhu Ha,Li Liu,David L. Williams,David L. Williams,Chuanfu Li,Chuanfu Li +16 more
TL;DR: In this paper, the authors demonstrated a role of lactate in HMGB1 lactylation and acetylation in macrophages during polymicrobial sepsis and found that macrophage can uptake extracellular lactate via monocarboxylate transporters (MCTs) to promote HMGB 1 lactylation via a p300/CBP-dependent mechanism.
Lactate and Immunosuppression in Sepsis.
TL;DR: Recent studies are summarized, showing that the activation of immune cells requires aerobic glycolytic metabolism and that lactate produced by aerobic Glycolysis may play an immunosuppressive role in sepsis.
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Lactate Suppresses Macrophage Pro-Inflammatory Response to LPS Stimulation by Inhibition of YAP and NF-κB Activation via GPR81-Mediated Signaling.
TL;DR: It is demonstrated that lactate exerts a previously unknown role in the suppression of macrophage pro-inflammatory cytokine production via GPR81 mediated YAP inactivation, resulting in disruption of YAP and NF-κB interaction and nuclear translocation in macrophages.
Enhanced Glycolytic Metabolism Contributes to Cardiac Dysfunction in Polymicrobial Sepsis.
Zhibo Zheng,He Ma,Xia Zhang,Fei Tu,Xiaohui Wang,Tuanzhu Ha,Min Fan,Li Liu,Jingjing Xu,Kaijiang Yu,Ruitao Wang,John Kalbfleisch,Race L. Kao,David E. Williams,Chuanfu Li +14 more
TL;DR: Glycolytic metabolism plays an important role in mediating sepsis-induced septic cardiomyopathy and the mechanisms may involve regulation of inflammatory response and apoptotic signaling.
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Cardiomyocyte-specific deficiency of HSPB1 worsens cardiac dysfunction by activating NFκB-mediated leucocyte recruitment after myocardial infarction.
Yana Wang,Jiali Liu,Qiuyue Kong,Hao Cheng,Fei Tu,Peng Yu,Ying Liu,Xiaojin Zhang,Chuanfu Li,Yuehua Li,Xinxu Min,Shuya Du,Zhengnian Ding,Li Liu +13 more
TL;DR: Data suggest that HSPB1 acts as a negative regulator of NFκB-mediated leucocyte recruitment and the subsequent inflammation in cardiomyocytes, which is required for wound healing after MI and could be a target for myocardial repair in MI patients.
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