破骨细胞分泌特定阶段的关键分子,调节破骨细胞与成骨细胞之间的交流

IF 4.5 2区 生物学 Q2 CELL BIOLOGY Journal of Cellular Physiology Pub Date : 2024-11-28 DOI:10.1002/jcp.31484
Yi-fei Fu, Shu-wen Shi, Jun-jie Wu, Zheng-dong Yuan, Lei-sheng Wang, Hao Nie, Zheng-yu Zhang, Xian Wu, Yue-chun Chen, Hui-bo Ti, Ke-yue Zhang, Dong Mao, Jun-xing Ye, Xia Li, Feng-lai Yuan
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引用次数: 0

摘要

在骨代谢紊乱的大多数病例中,如骨质疏松症和骨软化症,这些病症通常归因于破骨细胞功能失调,导致它们被普遍定性为 "破坏者"。除了广泛记载的成骨细胞指导破骨细胞骨吸收的调节过程外,越来越多的证据表明,破骨细胞也通过直接和间接机制反过来影响成骨细胞的骨形成。众所周知,破骨细胞的分化包括几个阶段,每个阶段都有特定的细胞特征和功能。这些阶段分泌的特定关键分子在介导破骨细胞与成骨细胞的交流中发挥着关键作用。在这篇综述中,我们描述了破骨细胞分化的不同阶段,并回顾了参与破骨细胞-成骨细胞通讯的特定阶段关键分子。我们强调,详细了解这些过程和分子机制有助于开发治疗骨代谢疾病的新方法。
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Osteoclast Secretes Stage-Specific Key Molecules for Modulating Osteoclast–Osteoblast Communication

In most cases of bone metabolic disorders, such as osteoporosis and osteomalacia, these conditions are often attributed to dysfunctional osteoclasts, leading to their common characterization as “destructors.” In addition to the widely documented regulatory process where osteoblasts direct osteoclastic bone resorption, there is increasing evidence suggesting that osteoclasts also in turn influence osteoblastic bone formation through direct and indirect mechanisms. It is well-known that differentiation of osteoclasts involves several stages, each characterized by specific cellular features and functions. Stage-specific key molecules secreted during these stages play a critical role in mediating osteoclast–osteoblast communication. In this review, we described the different stages of osteoclast differentiation and reviewed stage-specific key molecules involved in osteoclasts-osteoblasts communication. We highlighted that a detailed understanding of these processes and molecular mechanism could facilitate the development of novel treatments for bone metabolic disorders.

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来源期刊
CiteScore
14.70
自引率
0.00%
发文量
256
审稿时长
1 months
期刊介绍: The Journal of Cellular Physiology publishes reports of high biological significance in areas of eukaryotic cell biology and physiology, focusing on those articles that adopt a molecular mechanistic approach to investigate cell structure and function. There is appreciation for the application of cellular, biochemical, molecular and in vivo genetic approaches, as well as the power of genomics, proteomics, bioinformatics and systems biology. In particular, the Journal encourages submission of high-interest papers investigating the genetic and epigenetic regulation of proliferation and phenotype as well as cell fate and lineage commitment by growth factors, cytokines and their cognate receptors and signal transduction pathways that influence the expression, integration and activities of these physiological mediators. Similarly, the Journal encourages submission of manuscripts exploring the regulation of growth and differentiation by cell adhesion molecules in addition to the interplay between these processes and those induced by growth factors and cytokines. Studies on the genes and processes that regulate cell cycle progression and phase transition in eukaryotic cells, and the mechanisms that determine whether cells enter quiescence, proliferate or undergo apoptosis are also welcomed. Submission of papers that address contributions of the extracellular matrix to cellular phenotypes and physiological control as well as regulatory mechanisms governing fertilization, embryogenesis, gametogenesis, cell fate, lineage commitment, differentiation, development and dynamic parameters of cell motility are encouraged. Finally, the investigation of stem cells and changes that differentiate cancer cells from normal cells including studies on the properties and functions of oncogenes and tumor suppressor genes will remain as one of the major interests of the Journal.
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