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破骨细胞分化的新调控机制。

New regulation mechanisms of osteoclast differentiation.

机构信息

Department of Cell Signaling, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.

出版信息

Ann N Y Acad Sci. 2011 Dec;1240:E13-8. doi: 10.1111/j.1749-6632.2011.06373.x.

Abstract

Osteoclasts play a crucial role in both physiological and pathological bone resorption. It is, thus, of compelling importance to understand the molecular mechanisms of osteoclast regulation. Because receptor activator of nuclear factor-κB ligand (RANKL) is the key cytokine that induces osteoclast differentiation, we have focused on the investigation of RANKL signaling and RANKL-expressing cells. Here, we summarize the recent advances in the understanding of osteoclastogenic signaling and the cells that express RANKL in the context of osteoimmunology. The scope of osteoimmunology has been extended to now encompass a wide range of molecular and cellular interactions, and its framework provides a scientific basis for future therapeutic approaches to diseases related to the bone and/or immune systems.

摘要

破骨细胞在生理和病理骨质吸收中都发挥着关键作用。因此,了解破骨细胞调节的分子机制至关重要。由于核因子-κB 受体激活剂配体(RANKL)是诱导破骨细胞分化的关键细胞因子,我们一直专注于研究 RANKL 信号转导和表达 RANKL 的细胞。在此,我们总结了在骨免疫学背景下对破骨细胞生成信号转导和表达 RANKL 的细胞的最新认识进展。骨免疫学的范围已经扩展到包含广泛的分子和细胞相互作用,其框架为与骨骼和/或免疫系统相关疾病的未来治疗方法提供了科学依据。

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