THE RANK AND RANKL NEXUS – MOLECULAR ASPECTS

Javeria Khan, Devaratnamma Mv, Asma Naaz, Pooja Deshkar, Sahiti Soni, Sumanya Bandi
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Abstract

RANKL are the chemical mediators secreted by the resident cells of the connective tissue and in the mileau of periodontium they are released during the process of bone turnover either for bone remodelling during orthodontic tooth movement, normal masticatory force bearing, age related changes or for bone resorption due to pathological reasons where plaque influences the cells of inflammation to release PGE2, IL-1 and TNF alpha. These RANKL act on the circulating pre osteoclasts or monocyte macrophage cells which under the influence of M-CSF will start to colacase to form multinucleated osteoclasts that will resorb the bone. Thus, for these various changes to occur in the macrophages and preosteoclasts there will be a need of transcription factors like NFK฀, NFATc1, cFos and others. To understand intracellular mechanisms when RANKL binds onto the trimeric receptor RANK which leads to a better understanding of therapeutic management to deal with pathological bone destructive disease, so we have consolidated this narrative review.
等级与等级关系--分子方面
RANKL 是由结缔组织的常驻细胞分泌的化学介质,在牙周膜中,它们在骨转换过程中释放,或是在正畸牙齿移动、正常咀嚼受力、年龄相关变化时用于骨重塑,或是由于病理原因引起的骨吸收,即牙菌斑影响炎症细胞释放 PGE2、IL-1 和 TNF alpha。这些 RANKL 会作用于循环中的前破骨细胞或单核巨噬细胞,在 M-CSF 的影响下,这些细胞会开始钙化,形成多核破骨细胞,从而吸收骨质。因此,巨噬细胞和前破骨细胞要发生这些变化,就需要 NFK↪CN_E00↩、NFATc1、cFos 等转录因子的参与。为了了解当 RANKL 结合到三聚受体 RANK 上时的细胞内机制,从而更好地了解治疗方法,以应对病理性骨破坏性疾病,我们整理了这篇叙述性综述。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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