A SHORT COURSE IN THE MODELING OF CHEMOTAXIS

Lesion progression
Smooth muscle cells (SMCs) also respond to chemical signals produced during
the accumulation of oxLDL, foam cells, and debris. SMCs migrate around the lesion
to form a fibromuscular cap overlaying the plaque. This process is also mediated
by chemo-attractants which entice SMCs into the region as well as chemo-inhibitors
that keep the SMCs outside of the lesion core. The fibrofatty atherosclerotic plaque
is characterized by a fibrous cap of SMCs, poorly formed connective tissue and, in
some cases, lipid filled macrophages due to continued influx of leukocytes. The cap
covers the core which contains dead cells, foam cells, and potentially nectrotic tissue.
As described in the introduction, remodeling occurs that initially results in the
abluminal expansion of the arterial wall followed by eventual luminal encroachment
as the cells, cell matrix, and debris accumulate in the plaque. The overlaying surface
becomes thrombogenic resulting in platelet adherence due to increase in expression
of platelet-endothelial-cell adhesion molecule 1. The thrombus can further diminish
or even completely occlude blood flow at this site [23].
Continued disease progression results in an advanced lesion described as a fi-
brous plaque. These types of plaques are characterized by a dense cap composed of
SMCs, collagen, elastin, and basement membrane fibers. These plaques often cause
moderate (40%–50%) to severe (> 90%) arterial occlusion. However, the danger
of clinically significant ischemia imposed by such a lesion has more to do with the
stability of the plaque (which is primarily determined by the composition of the
cap and the lipid core) than the degree of occlusion caused by the plaque [14, 4].
The cap may be uniformly thick which provides stability to the lesion; the SMCs
are the main arbiters of the integrity of the cap. A nonuniform cap, primarily one
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