Homophilic Interaction Between Transmembrane-JAM-A and Soluble JAM-A Regulates Thrombo-Inflammation: Implications for Coronary Artery Disease.

Genetic predisposition through single-nucleotide variation (SNV) influences circulatory soluble junctional adhesion molecule-A (sJAM-A) levels in coronary artery disease (CAD) patients. Homozygous carriers of the minor alleles (SNVs rs2774276, rs790056) show enhanced levels of thrombo-inflammatory sJAM-A. Both SNVs and sJAM-A are associated with worse prognosis for recurrent myocardial infarction in CAD patients.