Oxidative stress and bone marrow adipocytes: Molecular mechanisms and possible implications.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Redox homeostasis is crucial for maintaining cellular processes and is closely linked to human skeletal health. Prior research has demonstrated that oxidative stress is important for regulating osteoblast and osteoclast differentiation in the bone microenvironment, leading to a reduction in bone mass and skeletal degradation. The bone marrow is a complex niche containing various cell types, including bone marrow adipocytes (BMAs), which engage in dynamic interplay with osteo-associated cells through processes governed by redox equilibrium within the marrow compartment. During aging, a decrease in osteoblasts coincides with an increase in BMAs counts. Evidence suggests that oxidative stress influences the differentiation of BMAs, leading to the accumulation of bone marrow adipose tissue (BMAT) and contributing to bone remodeling imbalances. The fate of BMAs is determined by a precise molecular network that involves transcription factors, epigenetic regulators, and ncRNAs. The expansion of BMAT affects the commitment and differentiation of bone marrow-derived mesenchymal stem cells (BMSCs), resulting in poor osteoblast differentiation, enhancing osteoclast differentiation and function, and accelerating bone loss. Consequently, elucidating oxidative stress dynamics in pathological marrow states and delineating their correlation with aberrant BMAs differentiation emerges as a resea

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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