Stroe-Ionescu Alexandra-Ştefania, Tǎnase Alina Daniela, Rotaru Ionela, Goanțǎ Janina-Georgiana, Pǎtraşcu Ana Maria, Boldeanu Mihail Virgil, Assani Mohamed-Zakaria, Siloși Isabela, Boldeanu Lidia, Maria Daniela-Teodora
Doctoral School, University of Medicine and Pharmacy of Craiova, 200349 Craiova, Romania.
Department of Hematology and Bone Marrow Transplantation, Fundeni Clinical Institute Bucharest, 022328 Bucharest, Romania.
Int J Mol Sci. 2025 Jun 11;26(12):5618. doi: 10.3390/ijms26125618.
In patients diagnosed with multiple myeloma (MM), the primary complaints at the time of diagnosis are often related to bone involvement, significantly impacting quality of life and increasing both morbidity and mortality. Obesity is associated with a chronic inflammatory state that results in the production of various cytokines and adipokines, which may promote bone destruction. Adiponectin, an adipokine predominantly secreted by adipocytes, is notably diminished in circulation among individuals with obesity, a phenomenon that has also been observed in MM. This reduction may contribute to the disruption of an already compromised bone architecture. The increase in adipose tissue is associated with heightened leptin production, a key adipokine, which can play a significant role in the pathophysiology of MM and its related bone complications. Obesity is associated with hyperinsulinemia and increased levels of free IGF-1. In MM, IGF-1 plays a critical role as a growth factor, produced by both myeloma cells and osteoclasts within the bone marrow microenvironment. Our gathered data indicates a significant relationship between the adipokines produced by adipose tissue and the bone matrix, particularly in the context of obesity and MM. However, it is important to note that the existing body of research on this topic is relatively sparse, with the majority of studies conducted on murine models rather than human subjects. This limitation highlights a critical need for further investigation to elucidate the precise mechanisms that contribute to bone destruction under these conditions.
在被诊断为多发性骨髓瘤（MM）的患者中，诊断时的主要主诉通常与骨受累有关，这对生活质量有显著影响，并增加了发病率和死亡率。肥胖与慢性炎症状态相关，会导致多种细胞因子和脂肪因子的产生，这可能促进骨质破坏。脂联素是一种主要由脂肪细胞分泌的脂肪因子，在肥胖个体的循环中显著减少，这种现象在MM患者中也有观察到。这种减少可能导致本已受损的骨结构遭到破坏。脂肪组织的增加与关键脂肪因子瘦素的产生增加有关，瘦素在MM及其相关骨并发症的病理生理学中可能起重要作用。肥胖与高胰岛素血症和游离胰岛素样生长因子-1（IGF-1）水平升高有关。在MM中，IGF-1作为一种生长因子发挥关键作用，由骨髓微环境中的骨髓瘤细胞和破骨细胞产生。我们收集的数据表明，脂肪组织产生的脂肪因子与骨基质之间存在显著关系，尤其是在肥胖和MM的背景下。然而，需要注意的是，关于这一主题的现有研究相对较少，大多数研究是在小鼠模型而非人类受试者上进行的。这一局限性凸显了进一步研究以阐明在这些情况下导致骨质破坏的确切机制的迫切需求。
