Sepsis-Induced Endothelial Barrier Dysfunction: Mechanisms, Pathology, and Therapeutic Advances

Area of Science:

• Pathophysiology
• Immunology
• Vascular Biology

Background:

• Sepsis is a critical illness with high mortality, driven by systemic inflammation and endothelial dysfunction.
• Endothelial barrier impairment in sepsis leads to multiorgan failure and microcirculatory disturbances.

Purpose of the Study:

• To comprehensively review the pathological mechanisms of sepsis-induced endothelial dysfunction.
• To discuss emerging therapeutic strategies for sepsis management.

Main Methods:

• Literature review of sepsis pathophysiology.
• Analysis of molecular mechanisms of endothelial cell injury.
• Overview of current and novel therapeutic interventions.

Main Results:

• Sepsis involves endothelial glycocalyx degradation, increased vascular permeability, and endothelial cell death (apoptosis, pyroptosis, ferroptosis).
• Coagulopathy and immune cell interactions exacerbate inflammation and endothelial damage.
• Therapeutic strategies include glycocalyx protectants, anti-inflammatory agents, and anticoagulants.

Conclusions:

• Understanding sepsis-induced endothelial dysfunction is crucial for developing effective treatments.
• Targeting endothelial protection, inflammation, and coagulation holds promise for improving sepsis patient outcomes.
• Further clinical translation of therapeutic approaches is needed.