Di Bartolo Belinda A, Kavurma Mary M
Heart Research Institute, Sydney, NSW 2042, Australia.
Curr Pharm Des. 2014;20(37):5853-61. doi: 10.2174/1381612820666140212205455.
Receptor activator of nuclear factor-κB ligand (RANKL) is a member of the tumour necrosis factor family important in bone remodelling. Recent evidence suggest that calcification in the vessel wall is equivalent to mechanisms mediating bone formation. This review highlights the role of RANKL in vascular arterial calcification. Here, the relationship between RANKL, osteoprotegerin (OPG) and tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) is discussed. Furthermore, we focus on the regulatory mechanisms mediating RANKL gene expression and transcription in cells of the vessel wall. A better understanding of RANKL-mediated signalling may help develop more sophisticated cell-based therapies to inhibit calcification of the vessel wall.
核因子κB受体激活剂配体（RANKL）是肿瘤坏死因子家族的成员，在骨重塑中起重要作用。最近的证据表明，血管壁钙化等同于介导骨形成的机制。本综述重点介绍了RANKL在血管动脉钙化中的作用。在此，讨论了RANKL、骨保护素（OPG）和肿瘤坏死因子相关凋亡诱导配体（TRAIL）之间的关系。此外，我们关注介导血管壁细胞中RANKL基因表达和转录的调控机制。更好地理解RANKL介导的信号传导可能有助于开发更复杂的基于细胞的疗法来抑制血管壁钙化。
