The relationship between bone marrow adipose tissue and bone metabolism in postmenopausal osteoporosis

• Published in: Cytokine & growth factor reviews Vol. 52; pp. 88 - 98
• Main Authors: Li, Jiao, Chen, Xiang, Lu, Lingyun, Yu, Xijie
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.04.2020
• Subjects: Advanced Basic Science; Bone metabolism; Estrogen withdrawal; Marrow adipose tissue; Postmenopausal osteoporosis; RANKL; JNK; OPG; RANK; CTGF; NF-κB; MSCs; TZDs; GM-CSF; FSH; SOST; LepR; CMKLR1; IONPs; IL; ERα; Dio2; MAPK; Bone metabolism; PPARγ; FoxC2; FFAs; TRAF6; ROS; rMAT; PMOP; MAT; BMAs; UCP1; NFATc1; WAT; Postmenopausal osteoporosis; BMMs; OVX; DPP4; PtNPs; cMAT; Estrogen withdrawal; PRDM16; BMD; TGF-β; SNS; Runx2; Marrow adipose tissue; EVs; C/EBP alpha; PGC-1α; GNPs; AdipoR; PA; CYLD; FABP4; TNF-α; BAT; HSCs; thiazolidinediones; estrogen withdrawal; receptor-associated factor 6; gold nanoparticles; platinum nanoparticles; Bone marrow adipocytes; iron oxide nanoparticles; sclerostin; uncoupling protein 1; CCAAT-enhancer-binding protein α; white adipose tissue; estrogen receptor alpha; forkhead box C2; fatty acid binding protein 4; free fatty acids; cylindromatosis; mitogen-activated protein kinase; deiodinase 2; peroxisome proliferator-activator receptor gamma; adiponectin receptor; tumor growth factor beta; bone marrow mesenchymal cells; extracellular vesicles; brown adipose tissue; hematopoietic stem cells; bone mineral density; constitutive marrow adipose tissue; marrow adipose tissue; c-Jun N-terminal kinase; regulated marrow adipose tissue; nuclear factor-κB; connective tissue growth factor; bone metabolism; osteoprotegerin; bone marrow monocytes/macrophages; granulocyte/ macrophage colony stimulating factor; receptor activator of nuclear factor-κB ligand; postmenopausal osteoporosis; chemokine-like receptor 1; tumor necrosis factor alpha; reactive oxygen species; interleukin; follicle-stimulating hormone; paltimic acid; leptin receptor; sympathetic nervous system; nuclear factor of activated T cells 1; receptor activator of nuclear factor-κB; positive regulatory domain containing 16; peroxisome proliferator activated receptor gamma coactivator 1 alpha; runt-related transcript factor 2; dipeptidyl peptidase 4; ovariectomy
• ISSN: 1359-6101; 1879-0305
• DOI: 10.1016/j.cytogfr.2020.02.003

[Display omitted] •With an aging population, postmenopausal osteoporosis (PMOP) has become a global public health issue.•Abnormal expansion of marrow adipose tissue (MAT) plays a crucial role in the onset and progression of PMOP.•Emerging therapeutic methods targeting MAT are confirmed to be effective in improving bone mass.•Further studies in this area will uncover the pathogenesis and provide additional therapeutic targets for PMOP. Postmenopausal osteoporosis (PMOP) is a prevalent skeletal disorder associated with menopause-related estrogen withdrawal. PMOP is characterized by low bone mass, deterioration of the skeletal microarchitecture, and subsequent increased susceptibility to fragility fractures, thus contributing to disability and mortality. Accumulating evidence indicates that abnormal expansion of marrow adipose tissue (MAT) plays a crucial role in the onset and progression of PMOP, in part because both bone marrow adipocytes and osteoblasts share a common ancestor lineage. The cohabitation of MAT adipocytes, mesenchymal stromal cells, hematopoietic cells, osteoblasts and osteoclasts in the bone marrow creates a microenvironment that permits adipocytes to act directly on other cell types in the marrow. Furthermore, MAT, which is recognized as an endocrine organ, regulates bone remodeling through the secretion of adipokines and cytokines. Although an enhanced MAT volume is linked to low bone mass and fractures in PMOP, the detailed interactions between MAT and bone metabolism remain largely unknown. In this review, we examine the possible mechanisms of MAT expansion under estrogen withdrawal and further summarize emerging findings regarding the pathological roles of MAT in bone remodeling. We also discuss the current therapies targeting MAT in osteoporosis. A comprehensive understanding of the relationship between MAT expansion and bone metabolism in estrogen deficiency conditions will provide new insights into potential therapeutic targets for PMOP.