Runx2相关微RNAs在慢性肾脏病血管钙化中作用的研究进展

    Research advances on the role of Runx2-related miRNAs in vascular calcification of chronic kidney disease

    • 摘要: 血管钙化是慢性肾脏病患者心血管病死亡的主要原因。目前研究认为慢性肾脏病血管钙化不仅仅是磷酸钙晶体在血管壁的异位沉积,其形成与骨矿化具有相似的机制,平滑肌细胞在血管钙化中起关键作用。充分的证据表明runt相关转录因子2(runt-related transcription factor2,Runx2)是血管平滑肌细胞成骨分化和钙化的必需调节因子。近年来,多种微RNAs被确定为血管钙化过程中血管平滑肌细胞分化、表型转换、增殖、凋亡、细胞因子产生和基质沉积的关键调节因子。因此,本综述主要讨论调控Runx2表达的相关微RNAs在平滑肌细胞成骨分化中的作用。由于血管钙化的确切机制仍未完全阐明,更好地理解微RNAs参与血管钙化可能推动治疗血管钙化的新型疗法。

       

      Abstract: Vascular calcification(VC)is a major cause of cardiovascular mortality in patients with chronic kidney disease(CKD). Current studies suggest that VC of CKD is not simply an ectopic deposition of calcium phosphate crystals in vascular wall. Formation of calcification has a similar mechanism to bone mineralization and smooth muscle cells play a key role in VC. Sufficient evidence suggested that Runx2 is an essential regulator of osteogenic differentiation and calcification in vascular smooth muscle cells. In recent years, multiple microRNAs have been identified as key regulators for differentiation of vascular smooth muscle cell, phenotypic switching, proliferation, apoptosis, cytokine production and matrix deposition during VC. This review focused upon the role of relevant microRNAs regulating Runx2 expression in osteogenic differentiation of smooth muscle cells. Since the exact mechanism of VC has remained largely elusive, a better understanding of microRNA involvement in VC may help to design novel therapies for VC.

       

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