激素性股骨头坏死（SONFH）是一种以骨髓微环境长期失衡为核心特征的非创伤性骨坏死性疾病，其发生发展过程难以仅用血供障碍或骨组织坏死加以解释。Adipoq⁺骨髓间充质干细胞（MALP）作为骨髓特异性的间充质细胞亚群，在骨髓稳态调控、血管重建及骨重塑过程中发挥重要作用，但其在SONFH中的潜在功能及病理意义尚缺乏系统阐释。本文将"卫虚-血瘀-髓痿"理论融入近年关于MALP的研究进展，从骨髓微环境整体失衡的视角，对MALP在SONFH发生发展中的可能作用机制进行阐述。MALP在激素性股骨头坏死中并非单纯的脂肪生成相关细胞，而是贯穿疾病不同阶段、深度参与骨髓微环境重构的重要调控节点：在"卫虚"阶段，长期或大剂量使用糖皮质激素可诱导MALP异常扩增，骨髓稳态调控能力下降；在"血瘀"阶段，MALP通过分泌血管调控因子参与血管稳态调节，其功能失衡可影响微循环重建，同时以核因子κB受体活化因子配体（RANKL）依赖性方式显著促进破骨细胞生成，推动血管功能障碍与骨吸收增强在骨髓微环境中的耦合放大；在"髓痿"阶段，MALP进一步向脂肪细胞和肌成纤维细胞转变，其稳态调控与修复支持功能持续衰减，骨髓修复潜能逐步耗竭，最终导致血供难以恢复和骨结构不可逆损伤。"卫虚—血瘀—髓痿"理论为从整体和动态角度理解MALP的阶段性功能转变提供了有力框架。围绕MALP可塑性及其微环境调控功能开展进一步研究，或可为SONFH的防治及中医药干预策略的优化提供新的理论依据和研究方向。

Steroid-induced osteonecrosis of the femoral head (SONFH) is a non-traumatic osteonecrotic disorder characterized by persistent disruption of the bone marrow microenvironment, a process that cannot be fully explained by vascular insufficiency or bone tissue necrosis alone. Emerging evidence has identified marrow adipogenic lineage precursors (MALPs) as a bone marrow-specific mesenchymal cell subpopulation that plays a critical role in regulating marrow homeostasis, vascular remodeling, and bone turnover. However, the functional significance and pathological involvement of MALPs in SONFH remain insufficiently defined.This review integrated recent advances in MALP biology with the traditional Chinese medicine (TCM) theory of Wei deficiency-blood stasis-marrow atrophy, and systematically analyze the potential stage-dependent roles of MALPs in the initiation and progression of SONFH from the perspective of global bone marrow microenvironmental imbalance. Available evidence suggests that during Wei deficiency stage, long-term or high-dose glucocorticoid use may induce abnormal expansion of MALPs, accompanied by impaired marrow homeostatic regulation. During the blood stasis stage, MALPs participate in vascular regulation through the secretion of angiogenic factors, while their functional dysregulation disrupts microcirculatory reconstruction and markedly promotes osteoclastogenesis in a receptor activator of nuclear ractor kappa B ligand (RANKL)-dependent manner, thereby amplifying the coupling between vascular dysfunction and excessive bone resorption. In the marrow atrophy stage, MALPs undergo further fate shifts toward adipocytes and myofibroblasts, resulting in sustained loss of regulatory and reparative capacity, progressive exhaustion of marrow regenerative potential, and ultimately irreversible vascular compromise and structural bone damage.Collectively, MALPs should not be regarded merely as adipogenesis-related cells in SONFH, but rather as central regulatory nodes that dynamically participate in bone marrow microenvironmental remodeling across disease stages. Wei deficiency-blood stasis-marrow atrophy theory provides a coherent conceptual framework for understanding the stage-specific functional transitions of MALPs in SONFH. Further investigation into MALP plasticity and microenvironmental regulatory functions may offer novel mechanistic insights and support the optimization of TCM -based therapeutic strategies for SONFH.