Cardiovascular Research Advance Access originally published online on February 15, 2008
Cardiovascular Research 2008 78(2):265-273; doi:10.1093/cvr/cvn039
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Diabetes and vessel wall remodelling: from mechanistic insights to regenerative therapies
1 IRCCS Multimedica, Milan, Italy
2 Bristol Heart Institute, University of Bristol, Bristol, UK
* Corresponding author. Tel/Fax: +44 117 9283904. E-mail address: madeddu{at}yahoo.com
Over the past two decades, extensive research has focused on arterial remodelling in both physiological and pathological ageing. The concept now describes the growth as well as the rearrangement of cellular components and extracellular matrix, resulting in either reduction or increase in vessel lumen. In diabetes, remodelling extends to capillaries, microvascular beds, and arteries of different calibre. This process is paralleled by accelerated atherosclerosis and accounts for an increased incidence of ischaemic complications. The incapacity of pre-existing and de novo formed collaterals to bypass atherosclerotic occlusions, combined with a decline in tissue capillary density, is responsible for the delayed recovery from ischaemia and ultimately leads to organ failure. The mechanisms of vascular remodelling are incompletely understood, but metabolic and mechanical factors seem to play an important role. Hyperglycaemia represents the main factor responsible for the fast progression of atherosclerosis as well as microangiopathy. However, intensive blood glucose control alone is insufficient to reduce the risk of macrovascular complications. Pharmacological control of oxidative stress and stimulation of nitric oxide release have proved to exert beneficial effects on vascular remodelling in experimental diabetic models. New approaches of regenerative medicine using vascular progenitor cells for the treatment of ischaemic disease have been shown to be safe and are now being tested for efficacy in pre-clinical and clinical trials.
KEYWORDS Diabetes; Remodelling; Angiogenesis; Endothelial progenitor cells; Advanced glycation end products
Time for primary review: 23 days
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