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Tissue factor pathways linking obesity and inflammation.

W Ruf1, F Samad

  • 1Wolfram Ruf, M.D., Professor, Department of Immunology and Microbial Science, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, Mail stop: SP258, Tel. 858/784-2748, Fax -8480, E-mail: ruf@uni-mainz.de, ruf@scripps.edu.

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Summary
This summary is machine-generated.

Tissue factor (TF) and its signaling through protease-activated receptors (PARs) promote obesity-related metabolic dysfunction. Targeting TF-PAR2 signaling may offer new strategies for treating metabolic syndrome and its complications.

Keywords:
PARsTF

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Area of Science:

  • Metabolic Syndrome Research
  • Obesity Pathophysiology
  • Inflammation and Immunity

Background:

  • Obesity is a primary driver of metabolic syndrome, including insulin resistance, type 2 diabetes, and liver steatosis.
  • Inflammation from immune cells and coagulation activation via tissue factor (TF) contribute to obesity-related metabolic abnormalities.
  • TF-mediated signaling through protease-activated receptors (PARs) is implicated in metabolic syndrome development.

Purpose of the Study:

  • To investigate the role of tissue factor (TF) and its signaling pathways in obesity-induced metabolic dysfunction.
  • To elucidate the specific contributions of adipocyte and hematopoietic TF-PAR2 signaling to metabolic syndrome components.
  • To explore the impact of TF-PAR2 signaling on hepatic metabolic regulation and inflammation.

Main Methods:

  • Utilized genetic and pharmacological approaches to study TF and PAR2 signaling in obesity models.
  • Examined TF-PAR2 signaling in adipose tissue, liver, and immune cells.
  • Analyzed gene expression related to metabolic pathways and inflammation in high-fat diet-fed mice.

Main Results:

  • Adipocyte TF-PAR2 signaling reduced metabolism and energy expenditure, contributing to diet-induced obesity.
  • Hematopoietic TF-PAR2 signaling drove adipose tissue inflammation, liver steatosis, and insulin resistance.
  • In the liver, PAR2 signaling upregulated genes for gluconeogenesis, lipogenesis, and inflammatory cytokines, while decreasing AMPK activation.

Conclusions:

  • TF-PAR2 signaling is a critical mediator of obesity-related metabolic syndrome.
  • Distinct roles of adipocyte versus hematopoietic TF-PAR2 signaling in metabolic dysfunction were identified.
  • Clinical markers of a TF-induced prothrombotic state may predict metabolic syndrome complications in obese patients.