作者
Julia V Busik, Maria Tikhonenko, Ashay Bhatwadekar, Madalina Opreanu, Nafissa Yakubova, Sergio Caballero, Danny Player, Takahiko Nakagawa, Aqeela Afzal, Jennifer Kielczewski, Andrew Sochacki, Stephanie Hasty, Sergio Li Calzi, Sungjin Kim, Shane K Duclas, Mark S Segal, Dennis L Guberski, Walter J Esselman, Michael E Boulton, Maria B Grant
发表日期
2009/12/21
期刊
Journal of Experimental Medicine
卷号
206
期号
13
页码范围
2897-2906
出版商
The Rockefeller University Press
简介
The present epidemic of diabetes is resulting in a worldwide increase in cardiovascular and microvascular complications including retinopathy. Current thinking has focused on local influences in the retina as being responsible for development of this diabetic complication. However, the contribution of circulating cells in maintenance, repair, and dysfunction of the vasculature is now becoming appreciated. Diabetic individuals have fewer endothelial progenitor cells (EPCs) in their circulation and these cells have diminished migratory potential, which contributes to their decreased reparative capacity. Using a rat model of type 2 diabetes, we show that the decrease in EPC release from diabetic bone marrow is caused by bone marrow neuropathy and that these changes precede the development of diabetic retinopathy. In rats that had diabetes for 4 mo, we observed a dramatic reduction in the number of nerve terminal …
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