Department of Stomatology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Hubei Key Laboratory of Oral and Craniomaxillofacial Development and Regeneration, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Front Cell Infect Microbiol. 2020 Sep 16;10:530190. doi: 10.3389/fcimb.2020.530190. eCollection 2020.
) has been recognized as a fatal pathogen to cause multiorgan failure by contributing to the formation of microthrombus. Coagulation and fibrinolysis systems have been found under the control of circadian clock genes. This study aimed to explore the correlation between and coagulation factor biosynthesis in infection. Mice were administered to induce sepsis, and HepG2 cells were also infected by . The expression of of hepatocytes was downregulated in the infection group, leading to the downregulation of coagulation factor VII (FVII) and the upregulation of the coagulation factor XII (FXII) and . Furthermore, we confirmed that the deficiency of contributed to the elevation of FVII and the decline in FXII by constructing BMAL1-deficiency () mice. The current result showed that BMAL1 regulates FVII directly. Thus, a novel insight into the coagulation abnormality in infection was gained that may optimize the treatment of sepsis by rescuing the expression of BMAL1 in the liver.
) 已被认为是一种致命的病原体，通过形成微血栓导致多器官衰竭。已经发现凝血和纤溶系统受生物钟基因的控制。本研究旨在探讨 与 感染中凝血因子生物合成的相关性。通过给予 诱导脓毒症，同时用 感染 HepG2 细胞。在 感染组中，肝细胞的 表达下调，导致凝血因子 VII (FVII)下调和凝血因子 XII (FXII) 和 的上调。此外，我们通过构建 BMAL1 缺陷 () 小鼠证实了 的缺乏导致 FVII 的升高和 FXII 的下降。目前的结果表明，BMAL1 直接调节 FVII。因此，获得了对 感染中凝血异常的新认识，这可能通过在肝脏中恢复 BMAL1 的表达来优化脓毒症的治疗。
