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Genetic basis for collateral circulatory insufficiency
Author(s) -
Faber James E
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.294.2
Subject(s) - collateral circulation , collateral , arteriogenesis , disease , ischemia , genome wide association study , collateral damage , genetic variation , medicine , biology , cardiology , gene , genetics , single nucleotide polymorphism , genotype , criminology , finance , sociology , economics
Native (pre‐existing) collaterals are rare arteriole anastomoses that interconnect two adjacent arterial trees, thus serving as endogenous bypass vessels. Despite their importance, nothing is known about when or how these vessels form. Furthermore, recent evidence indicates that the density and diameter of collaterals in tissues of healthy mice and humans evidences remarkable variation from as yet unknown mechanisms. This presentation will summarize evidence in mice for the following: The collateral circulation develops late embryonically and undergoes maturation early postnatally. Natural genetic variation exerts a profound effect on both processes, and on collateral remodeling in obstructive disease. This variation results in equally wide variation in the severity of tissue injury in models of stroke and peripheral artery disease. Several genes impacting collateral formation and remodeling have been identified. In addition, genome‐wide mapping studies have identified novel genetic loci and candidate genes linked to variation in collateral abundance. It is anticipated that identification of genetic polymorphisms affecting the native collateral circulation will lead to an understanding of the pathways controlling its formation, identify mechanisms underlying its wide variation, and possibly provide a means to predict risk‐severity for ischemic injury should obstructive disease develop.