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Role of CX3CL1/CX3CR1 Signaling Axis Activity in Osteoporosis

机译:CX3Cl1 / CX3CR1信号轴活性在骨质疏松症中的作用

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摘要

Osteoporosis is a civilization disease which is still challenging for contemporary medicine in terms of treatment and prophylaxis. It results from excessive activation of the osteoclastic cell line and immune cells like macrophages and lymphocytes. Cell-to-cell inflammatory information transfer occurs via factors including cytokines which form a complex network of cell humoral correlation, called cytokine network. Recently conducted studies revealed the participation of CX3CL1 chemokine in the pathogenesis of osteoporosis. CX3CL1 and its receptor CX3CR1 present unique properties among over 50 described chemokines. Apart from its chemotactic activity, CX3CL1 is the only chemokine which may function as an adhesion molecule which facilitates easier penetration of immune system cells through the vascular endothelium to the area of inflammation. The present study, based on world literature review, sums and describes convincing evidences of a significant role of the CX3CL1/CX3CR1 axis in processes leading to bone mineral density (BMD) reduction. The CX3CL1/CX3CR1 axis plays a principal role in osteoclast maturation and binding them with immune cells to the surface of the bone tissue. It promotes the development of inflammation and production of many inflammatory cytokines near the bone surface (i.e., TNF-α, IL-1β, and IL-6). High concentrations of CX3CL1 in serum are directly proportional to increased concentrations of bone turnover and inflammatory factors in human blood serum (TRACP-5b, NTx, IL-1β, and IL-6). Regarding the fact that acting against the CX3CL1/CX3CR1 axis is a potential target of immune treatment in osteoporosis, the number of available papers tackling the topic is certainly insufficient. Therefore, it seems justified to continue research which would precisely determine its role in the metabolism of the bone tissue as one of the most promising targets in osteoporosis therapy.
机译:骨质疏松症是一种文明疾病,仍然在治疗和预防方面对当代医学挑战。它是由于骨髓细胞系和免疫细胞的过度激活,如巨噬细胞和淋巴细胞等免疫细胞。细胞对细胞炎症信息转移通过包括细胞因子的因素发生,其形成复杂的细胞体液相关网络,称为细胞因子网络。最近进行的研究表明,CX3Cl1趋化因子参与骨质疏松症的发病机制。 CX3Cl1及其受体CX3CR1在50多个描述的趋化因子上具有独特的性质。除了其趋化活性外,CX3Cl1是唯一可以用作粘附分子的趋化因子,便于将免疫系统细胞更容易穿过血管内皮对炎症区域的粘附分子。本研究基于世界文献综述,总和和描述了CX3Cl1 / CX3CR1轴在导致骨矿物密度(BMD)减少的过程中的显着作用的令人信服的作用。 CX3Cl1 / CX3CR1轴在破骨细胞成熟中起主要作用,并将其与免疫细胞结合到骨组织的表面上。它促进了骨表面附近的许多炎症细胞因子的炎症和生产的发展(即TNF-α,IL-1β和IL-6)。血清中高浓度的CX3Cl1与人血清中的骨周转浓度和炎症因子增加成比例(TracP-5B,NTX,IL-1β和IL-6)。关于作用于CX3Cl1 / CX3CR1轴的事实是骨质疏松症免疫治疗的潜在目标,解决该主题的可用纸的数量肯定不足。因此,继续研究,继续研究,这将精确地确定其在骨组织的代谢中作为骨质疏松症治疗中最有前景的目标之一。

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