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The Role of Bone Marrow Microenvironment in Governing the Balance
between Osteoblastogenesis and Adipogenesis
Li Jiao 1 ;Liu Xingyu 1 ;zuo Bin 2 ;Zhang Li 3 ;
1 Department of Cell Biology, Zunyi Medical College, Zunyi, China ; 2 Department of Orthopedic Surgery, Xinhua Hospital, Shanghai
JiaoTong University School of Medicine (SJTUSM), Shanghai, China ; 3 Department of Orthopedics, Tenth People#cod#x00027;s
Hospital, Shanghai Tong Ji University, School of Medicine, Shanghai, China ;
Figure 1. BM microenvironment under pathological conditions. Aging-associated increase in ROS promotes NF-#cod#x003BA;B releasing from I#cod#x003BA;B and
subsequent translocation into nucleus where it binds to responsive element to activate transcription of inflammatory cytokines such as TNF#cod#x003B1;, Il-6 and MCP-1.
Elevated level of these inflammatory cytokines in BM results in immune cell infiltration from blood, such as T cells, monocytes and macrophages. CD40CD40L mediated Cellcell communication between T cells and BM stromal cells further enhances NF-#cod#x003BA;B signal, promoting stromal cells express more inflammatory cytokines.
Additional inflammatory cytokines such as TNF#cod#x003B1; and IL-1 secreted from stromal cells as well as infiltrated immune cells also stimulates ROS generation through
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Doi:10.14336/AD.2015.1206
mitochondrial and NADPH oxidase
system, forming a positive feedback loop that contributes to BM oxidative stress and chronic inflammation. These pathological
environmental signals shift MSC fate to favor adipocytes over osteoblasts. Accumulated fat further deteriorate BM microenvironment through secreted FFAs, inflammatory
cytokines and altered adipokine secretome. Besides, excessive FFAs generate more ROS while oxidation, initiating a vicious cycle that accelerates BM microenvironment
deterioration.