pubmed-article:18508460 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:18508460 | lifeskim:mentions | umls-concept:C0012634 | lld:lifeskim |
pubmed-article:18508460 | lifeskim:mentions | umls-concept:C0374711 | lld:lifeskim |
pubmed-article:18508460 | lifeskim:mentions | umls-concept:C0043240 | lld:lifeskim |
pubmed-article:18508460 | lifeskim:mentions | umls-concept:C0004153 | lld:lifeskim |
pubmed-article:18508460 | lifeskim:mentions | umls-concept:C0231175 | lld:lifeskim |
pubmed-article:18508460 | lifeskim:mentions | umls-concept:C1705181 | lld:lifeskim |
pubmed-article:18508460 | lifeskim:mentions | umls-concept:C0205227 | lld:lifeskim |
pubmed-article:18508460 | pubmed:dateCreated | 2008-5-29 | lld:pubmed |
pubmed-article:18508460 | pubmed:abstractText | As coronary artery disease (CAD) continues to be the primary cause of mortality, a more in-depth understanding of pathophysiology and novel treatments are being sought. The past two decades have established inflammation as a driving force behind CAD--from endothelial dysfunction to heart failure. Recent advances in stem/progenitor cell biology have led to initial applications of progenitor cells in CAD continuum and have revealed that atherosclerosis is, at least in part, a disease of failed endogenous vascular repair. Several key progenitor cell populations including endothelial progenitor cells (AC133+/CD34+ population), vascular progenitors (CD31+/CD45(low) population), KDR+ cells and other bone marrow subtypes are mobilized for vascular repair. However, age and risk factors negatively impact these cells even prior to clinical CAD. Sex-based differences in progenitor cell capacity for repair have emerged as a new research focus that may offer mechanistic insights into clinical CAD discrepancies between men and women. Quantifying injury and cell-based repair and better defining their interactions should enable us to halt or even prevent CAD by enhancing the repair side of the repair/injury equation. | lld:pubmed |
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