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Molecular Interaction of BMAT with Bone

机译：BMAT与骨骼的分子相互作用

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Purpose of Review Bone marrow adipose tissue (BMAT) is a distinct adipose tissue with diverse local and systemic effects, affecting both physiological processes and pathological conditions, including hematopoiesis, bone remodeling, osteoporosis, obesity, anorexia nervosa, diabetes, and cancer. BMAT increases with age and bone loss, while the significance of this phenomenon has been neglected until recently. Bone cells and BMAT are mutually connected in terms of bone remodeling and energy metabolism. It has been suggested that high BMAT is caused by a shift in bone marrow mesenchymal stromal cell (BMSC) differentiation in favor of adipogenesis, and BMAT promotes bone loss through direct or indirect interaction with bone cells. However, it remains unclear why osteoporosis accelerates BMAT accumulation and what is the role of BMAT in bone remodeling and particularly in bone loss. The purpose of this review is to present the latest published data on the role of BMAT in physiological bone processes and during osteoporosis progression. Recent Findings BMAT secretes numerous endocrine factors designated as adipokines as well as pro-inflammatory cytokines, which affect bone homeostasis through the regulation of osteoblast and osteoclast function. Most clinical data from osteoporotic patients demonstrate a negative relationship between BMAT and bone mass. Through technological advances in BMAT imaging, investigators are now able to quantify BMAT in humans and animal models. Pharmaceutical interventions targeting either bone loss or BMA expansion shed light in the understanding of the possible interactions between BMAT and bone cells. Summary A neglected feature of osteoporosis progression is BMAT development. BMAT appears as a “new tissue” with unique properties, which undoubtedly plays important physiological and pathological roles, but which remains insufficiently understood.
机译：审查骨髓脂肪组织（BMAT）是一种不同的脂肪组织，具有不同的局部和全身效应，影响生理过程和病理条件，包括血缺陷，骨质重塑，骨质疏松，肥胖症，厌食症神经系统，糖尿病和癌症。 BMAT随着年龄和骨质损失而增加，而这种现象的意义在最近忽略了忽视。骨细胞和BMAT在骨重塑和能量代谢方面相互连接。已经提出，高BMAT是由骨髓间充质细胞（BMSC）分化引起的，支持脂肪发生，BMAT通过与骨细胞的直接或间接相互作用促进骨质损失。然而，仍然清楚为什么骨质疏松症加速BMAT积累，BMAT在骨质损失中的作用是什么样的，特别是骨质损失。本综述的目的是介绍最新发表的BMAT在生理骨过程中的作用和骨质疏松症进展。最近的发现BMAT分泌了许多被指定为adipokines的内分泌因子以及促炎细胞因子，通过调节成骨细胞和骨质体功能来影响骨稳态。来自骨质疏松患者的大多数临床资料表现出BMAT和骨质之间的负面关系。通过BMAT成像的技术进步，调查人员现在能够在人类和动物模型中量化BMAT。在理解BMAT和骨细胞之间可能的相互作用时，靶向骨质损失或BMA扩展的药物干预措施。发明内容骨质疏松症进展的忽视特征是BMAT发育。 BMAT表现为“新组织”，具有独特的属性，无疑起到了重要的生理和病理作用，但仍然不充分理解。

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