Emerging roles of hematopoietic cells in the pathobiology of diabetic complications

被引:52
作者
Kojima, Hideto [1 ,2 ,3 ,4 ]
Kim, Jongoh [1 ,2 ,3 ]
Chan, Lawrence [1 ,2 ,3 ]
机构
[1] Baylor Coll Med, Dept Med, Houston, TX 77030 USA
[2] Baylor Coll Med, Dept Mol & Cellular Biol, Houston, TX 77030 USA
[3] Baylor Coll Med, Diabet & Endocrinol Res Ctr, Houston, TX 77030 USA
[4] Shiga Univ Med Sci, Dept Stem Cell Biol & Regenerat Med, Otsu, Shiga 5202192, Japan
基金
美国国家卫生研究院;
关键词
diabetes mellitus; complications; diabetic nephropathy; diabetic retinopathy; diabetic neuropathy; bone marrow; hematopoietic cells; ENDOTHELIAL PROGENITOR CELLS; MARROW-DERIVED CELLS; INSULIN-PRODUCING CELLS; OBESE DB/DB MICE; BONE-MARROW; RENAL INJURY; VASCULAR COMPLICATIONS; ADHESION MOLECULE-1; STEM-CELLS; PERIPHERAL-BLOOD;
D O I
10.1016/j.tem.2014.01.002
中图分类号
R5 [内科学];
学科分类号
100201 [内科学];
摘要
Diabetic complications encompass macrovascular events, mainly the result of accelerated atherosclerosis, and microvascular events that strike the eye (retinopathy), kidney (nephropathy), and nervous system (neuropathy). The traditional view is that hyperglycemia-induced dysregulated biochemical pathways cause injury and death of cells intrinsic to the organs affected. There is emerging evidence that diabetes compromises the function of the bone marrow (BM), producing a stem cell niche-dependent defect in hematopoietic stem cell mobilization. Furthermore, dysfunctional BM-derived hematopoietic cells contribute to diabetic complications. Thus, BM cells are not only a victim but also an accomplice in diabetes and diabetic complications. Understanding the underlying molecular mechanisms may lead to the development of new therapies to prevent and/or treat diabetic complications by specifically targeting these perpetrators.
引用
收藏
页码:178 / 187
页数:10
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