Coagulation factor XIII and atherothrombosis. A mini-review

Area of Science:

• Biochemistry and Molecular Biology
• Cardiovascular Research
• Thrombosis and Hemostasis

Background:

• Coagulation factor XIII (FXIII) is a transglutaminase crucial for fibrin crosslinking and extracellular matrix stabilization.
• FXIII influences fibrinolysis by incorporating alpha2 antiplasmin into the fibrin network.
• Previous studies noted elevated FXIII activity in hypertriglyceridemic individuals, correlating with hepatic protein synthesis markers.

Purpose of the Study:

• To investigate the relationship between insulin resistance (metabolic syndrome) and plasma factor XIII levels.
• To explore the dual pathogenic role of factor XIII in atherothrombosis.

Main Methods:

• Review and synthesis of existing literature on factor XIII activity, metabolic syndrome, and cardiovascular events.
• Analysis of reported correlations between factor XIII levels, insulin resistance markers, and clinical outcomes.
• Examination of the impact of factor XIII Val 34 leu polymorphism on cardiovascular protection in the context of metabolic syndrome.

Main Results:

• Recent literature confirms earlier findings of increased plasma factor XIII levels in subjects with insulin resistance (metabolic syndrome).
• The Val 34 leu polymorphism in FXIII activation offers protection against myocardial infarction and stroke, but this benefit is lost in insulin-resistant patients with high plasminogen activator inhibitor-1.
• Elevated FXIII activity may increase fibrin deposition and plaque burden while simultaneously reducing plaque vulnerability and embolization risk.

Conclusions:

• Factor XIII plays a complex, bivalent role in atherothrombosis.
• Increased FXIII activity associated with metabolic syndrome may promote fibrin persistence and plaque growth.
• FXIII's influence on plaque stability and embolization risk highlights its significance in cardiovascular disease pathogenesis.