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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.

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  • Authors+Show Affiliations

    ,

    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

    , , , , , , , , , , ,

    Source

    MeSH

    Atherosclerosis
    Endothelial Cells
    Gene Expression Regulation
    Genetic Predisposition to Disease
    Genome-Wide Association Study
    Humans
    Inflammation
    Models, Genetic
    Polymorphism, Single Nucleotide
    Stem Cells

    Pub Type(s)

    Journal Article
    Review

    Language

    eng

    PubMed ID

    21154163

    Citation

    Goldschmidt-Clermont, Pascal J., et al. "Inflammation, Stem Cells and Atherosclerosis Genetics." Current Opinion in Molecular Therapeutics, vol. 12, no. 6, 2010, pp. 712-23.
    Goldschmidt-Clermont PJ, Seo DM, Wang L, et al. Inflammation, stem cells and atherosclerosis genetics. Curr Opin Mol Ther. 2010;12(6):712-23.
    Goldschmidt-Clermont, P. J., Seo, D. M., Wang, L., Beecham, G. W., Liu, Z. J., Vazquez-Padron, R. I., ... Velazquez, O. C. (2010). Inflammation, stem cells and atherosclerosis genetics. Current Opinion in Molecular Therapeutics, 12(6), pp. 712-23.
    Goldschmidt-Clermont PJ, et al. Inflammation, Stem Cells and Atherosclerosis Genetics. Curr Opin Mol Ther. 2010;12(6):712-23. PubMed PMID: 21154163.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Inflammation, stem cells and atherosclerosis genetics. AU - Goldschmidt-Clermont,Pascal J, AU - Seo,David M, AU - Wang,Liyong, AU - Beecham,Gary W, AU - Liu,Zhao Jun, AU - Vazquez-Padron,Roberto I, AU - Dong,Chunming, AU - Hare,Joshua M, AU - Kapiloff,Michael S, AU - Bishopric,Nanette H, AU - Pericak-Vance,Margaret, AU - Vance,Jeffery M, AU - Velazquez,Omaida C, PY - 2010/12/15/entrez PY - 2010/12/15/pubmed PY - 2011/5/20/medline SP - 712 EP - 23 JF - Current opinion in molecular therapeutics JO - Curr. Opin. Mol. Ther. VL - 12 IS - 6 N2 - 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. SN - 2040-3445 UR - https://www.unboundmedicine.com/medline/citation/21154163/Inflammation,_stem_cells_and_atherosclerosis_genetics L2 - https://medlineplus.gov/atherosclerosis.html DB - PRIME DP - Unbound Medicine ER -