Abstract
Diabetes accelerates atherosclerosis through shortage of vascular regenerative cells derived from the bone marrow (BM). In addition, diabetes shifts the differentiation of BM progenitor cells to pro-calcific and smooth muscle phenotypes. In a paper published in Atherosclerosis, Fledderus et al. demonstrate that the accelerated atherosclerosis in diabetic ApoE−/− mice is associated with an increased amount of BM-derived smooth muscle cells in the plaques. The role of ApoE in the regulation of vascular BM progenitors may explain inconsistencies in the literature on the contribution of extraparietal cells to atherosclerotic lesions. Herein, the pathophysiological meaning of a deranged kinetic of smooth muscle progenitor cells in diabetes is discussed.
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