Regulation of smooth muscle cell accumulation in diabetes-accelerated atherosclerosis B. Askari, C.B. Renard and K.E. Bornfeldt Department of Pathology, University of Washington, Seattle, WA, USA Offrpirnt requests to: Karin E. Bornfeldt, Department of Pathology, Box 35470, University of Washington School of Medicine, Seattle, WA 98195-7470, USA. Fax: (206) 685 3018. e-mail: bornf@u.washington.edu
Summary. 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. Key words: Diabetes, Glucose, Growth factors, Macrovascular
complications, Non-esterified fatty acids |