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Updated: Feb 7, 2026

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Fli-1 Governs Pericyte Dysfunction in a Murine Model of Sepsis

Pengfei Li1, Yue Zhou1,2, Andrew J Goodwin3

  • 1Department of Pathology and Laboratory Medicine, Medical University of South Carolina, Charleston.

The Journal of Infectious Diseases
|July 28, 2018
PubMed
Abstract

Insights

Sepsis causes pericyte loss, a key factor in microvascular dysfunction. Targeting Friend leukemia virus integration 1 (Fli-1) in pericytes may prevent this loss and improve survival in sepsis.

Area of Science:

  • Cell Biology
  • Immunology
  • Vascular Biology

Background:

  • Pericytes are crucial mural cells within the microvasculature.
  • Pericyte loss is implicated in sepsis-induced microvascular dysfunction and mortality.
  • Mechanisms underlying pericyte loss during sepsis remain poorly understood.

Purpose of the Study:

  • To investigate the role of Friend leukemia virus integration 1 (Fli-1) in sepsis-induced pericyte loss.
  • To explore Fli-1 as a potential therapeutic target for sepsis.

Main Methods:

  • Utilized a cecal ligation and puncture (CLP) murine model of sepsis.
  • Assessed pericyte loss, vascular leak, and survival in wild-type and Fli-1 knockout mice.
  • Examined Fli-1 expression in lung pericytes in vivo and in vitro following LPS stimulation.

Main Results:

  • CLP induced significant pericyte loss in lungs and kidneys, reducing pericyte coverage.
  • Upregulated Fli-1 mRNA and protein levels were observed in pericytes during sepsis.
  • Fli-1 knockout in pericytes protected against CLP-induced pericyte loss, vascular leak, and improved survival.
  • Inhibition of Fli-1 reduced inflammatory cytokine and chemokine production and mitigated pyroptosis.

Conclusions:

  • Fli-1 plays a critical role in sepsis-induced pericyte loss and associated pathologies.
  • Targeting Fli-1 presents a promising therapeutic strategy for sepsis management.

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