Differential Role of Factor XIII in Acute Myocardial Infarction and Ischemic Stroke

Abstract

Factor XIII is a transglutaminase enzyme that plays a crucial role in hemostasis and wound healing. It crosslinks fibrin strands, stabilizing clots and promoting clot resistance to fibrinolysis. Additionally, Factor XIII has been found to have multiple other functions that extend beyond coagulation, including the regulation of inflammation and tissue repair processes. Emerging evidence suggests that Factor XIII may also have differential roles in acute myocardial infarction and ischemic stroke, two common cardiovascular events with significant morbidity and mortality. In acute myocardial infarction, Factor XIII has been implicated in promoting clot stability and reducing the risk of re-occlusion. In ischemic stroke, Factor XIII may also contribute to the pathogenesis of cerebral ischemia by promoting clot formation and exacerbating neuronal damage. Several studies have investigated the association between Factor XIII and these cardiovascular events, using various approaches such as genetic polymorphism analysis, animal models, and clinical data analysis. These studies have provided important insights into the role of Factor XIII in acute myocardial infarction and ischemic stroke, highlighting its potential as a therapeutic target for interventions aimed at improving outcomes in these conditions. In this review, we will summarize the current understanding of Factor XIII's role in acute myocardial infarction and ischemic stroke.

Keywords: acute myocardial infarction; biomarker; factor XIII; fibrin stabilizing factor; ischemic stroke; mortality; supplementation.

Figure 1

Structure, functions, and role of coagulation factor XIII in ischemic stroke and myocardial infarction. Factor XIII is an unusual blood coagulation factor, circulating as a heterotetramer composed of two catalytic A-subunits (A), two non-catalytic B-subunits (B), and activation peptides (APs). It is a member of the transglutaminase family with multiple functions, which extend its important role in the final stages of the coagulation cascade. Increased (↑) FXIII activity has been associated with an increased risk for ischemic stroke and myocardial infarction. In turn, low (↓) FXIII activity after an index event (acquired FXIII deficiency) relates to increased morbidity and mortality in both conditions. More research is needed to find out if and how FXIII supplementation may be beneficial in this regard.