Atherosclerosis in the context of hemostasis and neovascularization - Current state of knowledge

Area of Science:

• Cardiovascular Biology
• Pathogenesis Research
• Endothelial Function Studies

Background:

• Atherosclerosis is a progressive disease driven by endothelial dysfunction, often initiated by damage to the endothelial glycocalyx.
• Its complex pathogenesis involves biomechanical factors (blood pressure, shear stress) and biochemical pathways (lipid metabolism, monocyte-macrophage transition, immune responses, lipid accumulation, neovascularization, and coagulation activation).
• Recent findings confirm the possibility of atherosclerosis regression, yet the underlying mechanisms require further elucidation.

Purpose of the Study:

• To present current knowledge on atherosclerosis pathogenesis.
• To emphasize pro-atherogenic processes affecting the glycocalyx and endothelium.
• To highlight the roles of hemostasis, neovascularization, and epigenetic modifications in atherosclerosis.

Main Methods:

• Literature review of current scientific knowledge on atherosclerosis.
• Analysis of biomechanical and biochemical factors contributing to pathogenesis.
• Focus on endothelial glycocalyx integrity and its role in disease progression.

Main Results:

• Endothelial dysfunction, linked to glycocalyx damage, is a primary driver of atherosclerosis.
• Multiple factors including lipid disorders, inflammation, and coagulation contribute to plaque development.
• Epigenetic changes are emerging as critical factors in atherosclerosis development and potential regression.

Conclusions:

• Understanding the intricate pathogenesis of atherosclerosis, particularly glycocalyx and endothelial involvement, is crucial.
• Hemostasis, neovascularization, and epigenetic alterations are key areas for investigating atherosclerosis progression and regression.
• Further research into these mechanisms may reveal novel therapeutic targets for reversing atherosclerotic changes.