Things have changed: cell cycle dysregulation and smooth muscle cell dysfunction in atherogenesis.
The prevalence of coronary artery disease increases with age, and age itself is an independent risk factor for atherogenesis, suggesting that the biological milieu in aging populations is conducive to atheromatous lesion formation. Increased generation of reactive oxygen species and accrual of oxidative damage are likely factors in the atherogenic mechanism attributable to aging, yet the precise molecular processes underlying the age-associated events culminating in atherosclerotic lesion formation remain to be determined. Recent data suggest that changes in reactive oxygen species production are among the factors that contribute to vascular cell dysfunction associated with aging and that cell cycle events also become dysregulated at the same time, although we do not yet know the extent to which these two events are linked. Recent studies are discussed here that explore the link between aging, cell cycle events, and reactive oxygen species generation within the context of vascular cell biology and atherogenesis.
Patterson
Cam
C
Carolina Cardiovascular Biology Center, Department of Medicine, University of North Carolina, 5109C Neuroscience Building, Chapel Hill, NC 27599-7126, USA. cpatters@med.unc.edu
D000375:Aging / Q000473:pathology*; D000818:Animals; D002453:Cell Cycle / Q000502:physiology; D003324:Coronary Artery Disease / Q000473:pathology* / Q000503:physiopathology*; D003331:Coronary Vessels / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D009131:Muscle, Smooth, Vascular / Q000473:pathology* / Q000503:physiopathology*