Osteoblasts primarily mediate bone formation, maintain bone structure, and regulate bone mineralization, which plays an important role in bone remodeling. In the past decades, the roles of cytokines, signaling proteins, and transcription factors in osteoblasts have been widely studied. However, whether the energy metabolism of cells can be regulated by these factors to affect the differentiation and functioning of osteoblasts has not been explored in depth. In addition, the signaling and energy metabolism pathways are not independent but closely connected. Although energy metabolism is mediated by signaling pathways, some intermediates of energy metabolism can participate in protein post-translational modification. The content of intermediates, such as acetyl coenzyme A (acetyl CoA) and uridine diphosphate N-acetylglucosamine (UDP-N-acetylglucosamine), determines the degree of acetylation and glycosylation in terms of the availability of energy-producing substrates. The utilization of intracellular metabolic resources and cell survival, proliferation, and differentiation are all related to the integration of metabolic and signaling pathways. In this paper, the interaction between the energy metabolism pathway and osteogenic signaling pathway in osteoblasts and bone marrow mesenchymal stem cells (BMSCs) will be discussed.

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Background Osteoblasts and osteoclasts can regulate each other through the expression of a series of communication factors. In addition, the effects of p-Smad3 in different maturation stages osteoblasts on osteoclast proliferation, migration, differentiation, apoptosis and bone remodeling have not been clearly elucidated. Methods and results We collected conditioned media before and after osteoblast maturation, during which p-Smad3 was blocked or not blocked. The collected conditioned medium was used to interfere with osteoclast, and the proliferation, migration, maturation and differentiation of osteoclast, expression of osteoclast related molecules, and apoptosis of osteoclast were detected. At the same time, the conditioned medium from osteoclast was collected to interfere with osteoblasts and vascular endothelial cells, and the osteogenic ability of osteoblasts and the formation of vascular endothelial cells were detected to reflect the bone remodeling effect of osteoclast. The expression of related coupling molecules in osteoblasts and osteoclasts were detected by qPCR. Our study demonstrated that pre-osteoblasts primarily facilitated the migration, differentiation, and coupling of osteogenesis with osteoclasts. In contrast, matured osteoblasts primarily impeded osteoclast maturation, induced apoptosis, and facilitated coupling with angiogenesis. Additionally, p-Smad3 was found to positively regulate all of these processes. Conclusions The results showed thatosteoblasts impact the expression of several communication factors through p-Smad3 both before and after maturation. This shift in communication factors alters the cytological behavior of osteoclasts, causing them to transition from differentiation and osteogenesis coupling to apoptosis and angiogenesis coupling.