Oxidant stress and endothelial cell dysfunction

Area of Science:

• Cellular and Molecular Biology
• Physiology
• Pathophysiology

Background:

• Reactive oxygen species (ROS) are crucial signaling molecules at low levels but cause cellular injury at high concentrations.
• The vascular endothelium is a key target of oxidant stress, impacting vascular diseases.
• Oxidant stress alters endothelial permeability and leukocyte adhesion via signal transduction pathways.

Purpose of the Study:

• To review recent findings on the mechanisms of ROS signaling in endothelial dysfunction.
• To elucidate how ROS impairs endothelial barrier function and promotes leukocyte adhesion.
• To emphasize the regulation of adhesion molecules, cytoskeleton, and signal transduction.

Main Methods:

• Literature review of recent findings on ROS and endothelial function.
• Analysis of cellular and molecular mechanisms.
• Focus on signal transduction pathways and redox-regulated transcription factors.

Main Results:

• ROS signaling at higher concentrations leads to impaired endothelial barrier function.
• Oxidant stress promotes leukocyte adhesion to the endothelium.
• Alterations in cell-cell adhesion, cytoskeleton, and protein kinases are involved.

Conclusions:

• ROS play a dual role in cellular regulation, with detrimental effects at high concentrations on endothelial function.
• Understanding ROS mechanisms is critical for addressing vascular diseases.
• Further research on signal transduction and redox regulation is warranted.