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Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
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Related Experiment Video

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Isolation of Primary Mouse Lung Endothelial Cells
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Sepsis-Induced Endothelial Dysfunction: Permeability and Regulated Cell Death.

Wei Zhang1, Luofeng Jiang1, Xirui Tong1

  • 1Department of Burn Surgery, the First Affiliated Hospital of Naval Medical University, Shanghai, 200433, People's Republic of China.

Journal of Inflammation Research
|December 4, 2024
PubMed
Summary
This summary is machine-generated.

Sepsis severely impacts endothelial cells (ECs), compromising barrier function. This review explores EC damage mechanisms in sepsis, including glycocalyx and regulated cell death (RCD), to inform new therapies.

Keywords:
damage-associated proteinendothelial cellglycocalyxpermeabilityregulated cell deathsepsis

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Area of Science:

  • Cell Biology
  • Immunology
  • Pathophysiology

Background:

  • Sepsis is a life-threatening condition characterized by organ dysfunction due to a dysregulated host response to infection.
  • Endothelial cells (ECs) are crucial in sepsis pathogenesis, exhibiting compromised barrier function and regulated cell death (RCD).
  • The exact mechanisms driving sepsis-induced EC damage are not fully understood.

Purpose of the Study:

  • To review recent research on factors and mechanisms affecting EC permeability and RCD in sepsis.
  • To elucidate the underlying mechanisms of endothelial dysfunction in sepsis.
  • To provide insights for developing targeted small-molecule therapies.

Main Methods:

  • Literature review of recent research progress.
  • Focus on factors influencing ECs in septic conditions.
  • Analysis of various RCD pathways in ECs.

Main Results:

  • Identified key factors affecting EC permeability and RCD in sepsis.
  • Summarized the roles of glycocalyx and damage-associated molecular patterns (DAMPs).
  • Detailed various RCD forms in ECs: apoptosis, pyroptosis, ferroptosis, and autophagy.

Conclusions:

  • Endothelial dysfunction in sepsis involves complex interactions affecting EC permeability and RCD.
  • Understanding these mechanisms is vital for therapeutic development.
  • Targeting EC-specific pathways may lead to novel clinical treatments for sepsis.