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.

中文翻译：

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绝经后骨质疏松症中骨髓脂肪组织与骨代谢的关系。

绝经后骨质疏松症（PMOP）是与绝经相关的雌激素戒断相关的普遍骨骼疾病。PMOP的特征是骨量低，骨骼微体系结构恶化以及对脆性骨折的敏感性增加，从而导致残疾和死亡。越来越多的证据表明，骨髓脂肪组织（MAT）的异常扩增在PMOP的发生和发展中起着至关重要的作用，部分原因是骨髓脂肪细胞和成骨细胞都具有共同的祖先血统。MAT脂肪细胞，间充质基质细胞，造血细胞，成骨细胞和破骨细胞在骨髓中共存会产生一个微环境，该环境可使脂肪细胞直接作用于骨髓中的其他细胞类型。此外，公认的内分泌器官MAT 通过脂肪因子和细胞因子的分泌来调节骨骼重塑。尽管增加的MAT量与低骨量和PMOP骨折有关，但MAT与骨代谢之间的详细相互作用仍然未知。在这篇综述中，我们检查了雌激素戒断下MAT扩张的可能机制，并进一步总结了关于MAT在骨骼重塑中的病理作用的新发现。我们还将讨论针对骨质疏松症中MAT的当前疗法。对雌激素缺乏条件下MAT扩展与骨代谢之间关系的全面理解将为PMOP的潜在治疗靶点提供新的见解。MAT与骨骼代谢之间的详细相互作用仍然未知。在这篇综述中，我们检查了雌激素戒断下MAT扩张的可能机制，并进一步总结了关于MAT在骨骼重塑中的病理作用的新发现。我们还将讨论针对骨质疏松症中MAT的当前疗法。对雌激素缺乏症条件下MAT扩展与骨代谢之间关系的全面理解将为PMOP的潜在治疗靶点提供新的见解。MAT与骨骼代谢之间的详细相互作用仍然未知。在这篇综述中，我们检查了雌激素戒断下MAT扩张的可能机制，并进一步总结了关于MAT在骨骼重塑中的病理作用的新发现。我们还将讨论针对骨质疏松症中MAT的当前疗法。对雌激素缺乏条件下MAT扩展与骨代谢之间关系的全面理解将为PMOP的潜在治疗靶点提供新的见解。我们还将讨论针对骨质疏松症中MAT的当前疗法。对雌激素缺乏症条件下MAT扩展与骨代谢之间关系的全面理解将为PMOP的潜在治疗靶点提供新的见解。我们还将讨论针对骨质疏松症中MAT的当前疗法。对雌激素缺乏条件下MAT扩展与骨代谢之间关系的全面理解将为PMOP的潜在治疗靶点提供新的见解。