Publication: Regulation of smooth muscle cell accumulation in diabetes-accelerated atherosclerosis
Authors
Askari, B. ; Renard, C.B. ; Bornfeldt, K.E.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
Diabetes leads to accelerated formation/
progression of lesions of atherosclerosis. Cardiovascular
disease thus develops earlier in people with type 1 or
type 2 diabetes compared to people without diabetes,
and cardiovascular (macrovascular) disease is the major
cause of death in adults with diabetes. The molecular
and cellular mechanisms leading to diabetes-accelerated
atherosclerosis are not well understood. The arterial
smooth muscle cell (SMC), one of the three or four
principal cell types in atherosclerosis, has been
extensively studied over the years. Proliferation and
accumulation of SMCs are believed to play important
roles in the progression of macrophage-rich lesions to
fibroatheromas. Further progression of these atheromas
into complicated vulnerable lesions that are likely to
cause the acute clinical symptoms of atherosclerosis
(myocardial infarction and stroke) may involve cell
death and loss of SMCs from the fibrous cap of the
lesion.
Recent animal studies have shown that diabetes
causes a marked increase in SMC accumulation and
proliferation in atheromas. Hyperglycemia, advanced
glycation end-products, insulin and lipid abnormalities
associated with the diabetic environment have been
suggested to increase SMC accumulation. Indeed, it is
becoming increasingly clear that macrovascular disease
associated with diabetes is a multifactorial disease. We
review the factors and mechanisms that may regulate SMC proliferation and accumulation in different stages
of lesion progression in diabetes. We propose that lipid
abnormalities associated with diabetes can act in
combination with growth factors present in the diabetic
environment to increase SMC accumulation and
accelerate lesion progression.
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