Atherosclerosis as a disease of failed endogenous repair.
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.
Zenovich
Andrey G
AG
Center for Cardiovascular Repair, University of Minnesota, Minneapolis, MN 55455, USA.
Taylor
Doris A
DA
D015703:Antigens, CD / Q000502:physiology; D050197:Atherosclerosis / Q000150:complications / Q000503:physiopathology*; D003327:Coronary Disease / Q000453:epidemiology; D005298:Fertility; D006801:Humans; D013234:Stem Cells / Q000502:physiology; D020521:Stroke / Q000453:epidemiology; D014945:Wound Healing
D015703:Antigens, CD