Aging, inflammation, stem cells, and bone healing

被引:208
作者
Gibon, Emmanuel [1 ,2 ,3 ]
Lu, Laura [1 ]
Goodman, Stuart B. [1 ]
机构
[1] Stanford Univ, Dept Orthopaed Surg, R116,300 Pasteur Dr, Stanford, CA 94305 USA
[2] Univ Paris 07, Fac Med, Lab Biomecan & Biomat Osteo Articulaires, UMR CNRS 7052, 10 Ave Verdun, F-75010 Paris, France
[3] Univ Paris 05, Hop Cochin, APHP, Dept Orthopaed Surg, 27 Rue Faubourg St Jacques, F-75014 Paris, France
基金
美国国家卫生研究院;
关键词
AGE-RELATED-CHANGES; IN-VITRO EXPANSION; FRACTURE REPAIR; MACROPHAGE POLARIZATION; MURINE MACROPHAGES; OSTEAL MACROPHAGES; EXPERIMENTAL-MODEL; MOUSE MODEL; DONOR AGE; IFN-GAMMA;
D O I
10.1186/s13287-016-0300-9
中图分类号
Q813 [细胞工程];
学科分类号
100113 [医学细胞生物学];
摘要
Complex interactions among cells of the monocyte-macrophage-osteoclast lineage and the mesenchymal stem cell-osteoblast lineage play a major role in the pathophysiology of bone healing. Whereas the former lineage directs inflammatory events and bone resorption, the latter represents a source of cells for bone regeneration and immune modulation. Both of these lineages are affected by increasing age, which is associated with higher baseline levels of inflammatory mediators, and a significant reduction in osteogenic capabilities. Given the above, fracture healing, osteoporosis, and other related events in the elderly present numerous challenges, which potentially could be aided by new therapeutic approaches to modulate both inflammation and bone regeneration.
引用
收藏
页数:7
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