|
Inflammatory Mechanisms of Neointimal Hyperplasia
and Arterial Remodeling |
Myofibroblast migration into the intima followed by proliferation and matrix deposition (neointimal hyperplasia, NIH) stands as a central feature of early atherosclerosis, restenosis, and bypass graft failure. Most prior research focused on the biochemical mechanisms of NIH, though various mechanical forces on the arterial wall can also result is this fibroproliferative response. For example, intimal thickening and atherosclerosis tend to occur in areas of low wall shear stress such as the carotid bifurcation. Complete signaling pathways from biomechanical fluid forces to changes in arterial cell biology have not been completely dissected. Multiple lines of research suggest that NIH occurs by way of inflammatory dependent mechanisms. Our research to date supports the theory that inflammation (specifically pro-inflammatory cytokines such as TNF-± and IL-1) serves as pivotal modulators of NIH. We have recently explored the role of pro-inflammatory cytokines and positive arterial remodeling. Better understanding these mechanisms may lead to pro-and anti inflammatory prevention/treatment strategies to optimize blood vessel architecture in health and disease.
|
