• Welcome to Phoenix Rising!

    Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of, and finding treatments for, complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia, long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.

    To become a member, simply click the Register button at the top right.

Fibroblast growth factor-21 as a novel metabolic factor for regulating thrombotic homeostasis (Li et al, 2022)

SNT Gatchaman

Senior Member
New Zealand
Fibroblast growth factor-21 as a novel metabolic factor for regulating thrombotic homeostasis
Shuai Li, Haibo Jia, Zhihang Liu, Nan Wang, Xiaochen Guo, Muhua Cao, Fang Fang, Jiarui Yang, Junyan Li, Qi He, Rui Guo, Teng Zhang, Kai Kang, Zongbao Wang, Shijie Liu, Yukai Cao, Xinghao Jiang, Guiping Ren, Kai Wang, Bo Yu, Wei Xiao, Deshan Li

Fibroblast growth factor-21 (FGF-21) performs a wide range of biological functions in organisms. Here, we report for the first time that FGF-21 suppresses thrombus formation with no notable risk of bleeding. Prophylactic and therapeutic administration of FGF-21 significantly improved the degree of vascular stenosis and reduced the thrombus area, volume and burden.

We determined the antithrombotic mechanism of FGF-21, demonstrating that FGF-21 exhibits an anticoagulant effect by inhibiting the expression and activity of factor VII (FVII). FGF-21 exerts an antiplatelet effect by inhibiting platelet activation. FGF-21 enhances fibrinolysis by promoting tissue plasminogen activator (tPA) expression and activation, while inhibiting plasminogen activator inhibitor 1 (PAI-1) expression and activation. We further found that FGF-21 mediated the expression and activation of tPA and PAI-1 by regulating the ERK1/2 and TGF-β/Smad2 pathways, respectively. In addition, we found that FGF-21 inhibits the expression of inflammatory factors in thrombosis by regulating the NF-κB pathway.

Link | PDF