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lüll Atherosclerosis as a disease of failed endogenous repair Zenovich AG; Taylor DAFront Biosci 2008[May]; 13 (ä): 3621-36As 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.|Antigens, CD/physiology[MESH]|Atherosclerosis/complications/*physiopathology[MESH]|Coronary Disease/epidemiology[MESH]|Fertility[MESH]|Humans[MESH]|Stem Cells/physiology[MESH]|Stroke/epidemiology[MESH]|Wound Healing[MESH] |