Search

The article attempts to identify candidate loci responsible for genetic-dependent variation in collateral circulation. The authors reported that four quantitative trait loci (QTL) were derived for collateral number, including epistasis between two loci. They were also able to map a QTL that was identical with the strongest QTL for chromosome 7 collateral number. They concluded that collateral extent and remodeling are heritable complex traits.

The article presents a study which investigated the role of endothelial nitric oxide synthase (eNOS) in forming native collaterals and remodeling in obstructive disease by comparing the native collateral circulation in healthy tissue and collateral remodeling after femoral artery ligation (FAL) in wild-type and eNOS-knockedout (KO) mice. The results showed that perfusion after FAL fell in adult eNOS-KOs due to collateral loss during growth to adulthood. eNOS-KOs also has reduced collateral remodeling and angiogenesis as compared to wild-types.