title: Inflammation, stem cells and atherosclerosis genetics.
abstract: Atherosclerosis and its associated complications remain the primary cause of death in humans. Aging is the main contributor to atherosclerosis, compared with any other risk factor, yet the specific manner in which age increases risk (the 'aging-risk' mechanism) remains elusive. A novel concept for atherosclerosis risk implicates a lack of endothelial progenitor cell (EPC)-dependent arterial repair in the development of the disease that is secondary to exhaustion of repair-competent EPCs. Molecular evidence derived from genetic techniques indicates atherosclerotic lesions may begin to form as arterial repair fails, rather than merely following arterial injury. Thus, chronic arterial injury may overwhelm the ability of EPCs to maintain arterial homeostasis, particularly when EPCs capable of arterial repair become exhausted. Recent studies have reported genes identified using non-biased approaches (ie, genetic linkage studies and genome-wide association studies) that are associated with susceptibility for atherosclerosis and related thromboembolic disorders; these genes may be implicated in the control of arterial wall inflammation and EPC-mediated tissue repair. Most of the genes identified by using non-biased genomic techniques are associated with inflammation, immune response and stem cells. This review focuses on new genetic data in the field of atherosclerosis and arterial homeostasis.
authors.affiliation: University of Miami Leonard M Miller School of Medicine, Department of Medicine, Rosenstiel Medical Science Building, 1600 NW 10th Avenue, Miami, FL 33136, USA. pgoldschmidt@med.miami.edu
authors.forename: Pascal J
authors.initials: PJ
authors.lastname: Goldschmidt-Clermont
authors.forename: David M
authors.initials: DM
authors.lastname: Seo
authors.forename: Liyong
authors.initials: L
authors.lastname: Wang
authors.forename: Gary W
authors.initials: GW
authors.lastname: Beecham
authors.forename: Zhao Jun
authors.initials: ZJ
authors.lastname: Liu
authors.forename: Roberto I
authors.initials: RI
authors.lastname: Vazquez-Padron
authors.forename: Chunming
authors.initials: C
authors.lastname: Dong
authors.forename: Joshua M
authors.initials: JM
authors.lastname: Hare
authors.forename: Michael S
authors.initials: MS
authors.lastname: Kapiloff
authors.forename: Nanette H
authors.initials: NH
authors.lastname: Bishopric
authors.forename: Margaret
authors.initials: M
authors.lastname: Pericak-Vance
authors.forename: Jeffery M
authors.initials: JM
authors.lastname: Vance
authors.forename: Omaida C
authors.initials: OC
authors.lastname: Velazquez
mesh_terms: D050197:Atherosclerosis / Q000235:genetics* / Q000628:therapy; D042783:Endothelial Cells / Q000378:metabolism*; D005786:Gene Expression Regulation; D020022:Genetic Predisposition to Disease; D055106:Genome-Wide Association Study; D006801:Humans; D007249:Inflammation / Q000235:genetics*; D008957:Models, Genetic; D020641:Polymorphism, Single Nucleotide; D013234:Stem Cells / Q000378:metabolism*