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Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
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Updated: May 12, 2026

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FGL2-HDAC11 Drives Immunothrombosis via NETs-Mediated Endothelial Capillarization in MASLD Fibrosis.

Xitang Li1, Junjian Hu1, Suping Hai1

  • 1Department of Infectious Diseases Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, Hubei, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|May 10, 2026
PubMed
Summary

Metabolic dysfunction-associated steatotic liver disease (MASLD) involves immunothrombosis, where neutrophil extracellular traps (NETs) worsen liver fibrosis. Targeting the FGL2-HDAC11-NETs axis may treat MASLD without increasing bleeding risks.

Keywords:
fibrinogen like protein 2immunothrombosisliver fibrosismetabolic dysfunction‐associated steatotic liver diseaseneutrophil extracellular traps

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Area of Science:

  • Hepatology
  • Immunology
  • Vascular Biology

Background:

  • Metabolic dysfunction-associated steatotic liver disease (MASLD) often leads to liver fibrosis and cardiovascular issues.
  • The precise mechanisms connecting coagulation abnormalities to MASLD progression are not fully understood.

Purpose of the Study:

  • To investigate the role of immunothrombosis in MASLD-associated liver fibrosis.
  • To identify specific molecular pathways linking coagulation and liver disease progression.

Main Methods:

  • Analysis of liver tissues and plasma from MASLD patients and mouse models.
  • Pharmacological inhibition of coagulation pathways (dabigatran, aspirin) and genetic disruption of key proteins (FGL2).
  • Assessment of neutrophil extracellular traps (NETs) formation, endothelial cell function, and fibrotic markers.

Main Results:

  • Neutrophil extracellular traps (NETs) contribute to fibrin deposition, impaired liver microcirculation, and fibrosis in MASLD.
  • Fibrinogen-like protein 2 (FGL2) derived from neutrophils acts upstream of NETs formation via HDAC11.
  • Inhibiting FGL2 or NETs attenuated fibrosis and restored liver sinusoidal endothelial cell (LSEC) function without systemic bleeding.

Conclusions:

  • An immunothrombotic axis involving FGL2, HDAC11, and NETs drives liver fibrosis in MASLD.
  • This pathway links coagulation abnormalities to endothelial dysfunction in metabolic liver disease.
  • Targeting this axis offers a potential therapeutic strategy for MASLD with reduced bleeding risk.