期刊
OSTEOPOROSIS INTERNATIONAL
卷 25, 期 4, 页码 1197-1207出版社
SPRINGER LONDON LTD
DOI: 10.1007/s00198-013-2511-6
关键词
Bone fracture; Charcot osteoarthropathy; Diabetes; Neuropathy; RANKL/OPG; Vascular calcification
资金
- British Heart Foundation
- Diabetes Research and Wellness Foundation
- British Heart Foundation [RG/11/14/29056] Funding Source: researchfish
Emerging evidence from the last two decades has shown that vascular calcification (VC) is a regulated, cell-mediated process orchestrated by vascular smooth muscle cells (VSMCs) and that this process bears many similarities to bone mineralization. While many of the mechanisms driving VSMC calcification have been well established, it remains unclear what factors in specific disease states act to promote vascular calcification and in parallel, bone loss. Diabetes is a condition most commonly associated with VC and bone abnormalities. In this review, we describe how factors associated with the diabetic milieu impact on VSMCs, focusing on the role of oxidative stress, inflammation, impairment of the advanced glycation end product (AGE)/receptor for AGE system and, importantly, diabetic neuropathy. We also explore the link between bone and VC in diabetes with a specific emphasis on the receptor activator of nuclear factor kappa I-2 ligand/osteoprotegerin system. Finally, we describe what insights can be gleaned from studying Charcot osteoarthropathy, a rare complication of diabetic neuropathy, in which the occurrence of VC is frequent and where bone lysis is extreme.
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