低氧诱导因子2α可能作为治疗骨关节炎的一个新靶点
Hypoxia-inducible factor 2α may be a new target for the treatment of osteoarthritis
  
DOI:10.3969/j.issn.1006-7108.2019.06.033
中文关键词:  骨关节炎  低氧诱导因子2α  关节软骨
英文关键词:osteoarthritis  hypoxia-inducible factor 2α  articular cartilage
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作者单位
吴文彬 荣杰生* 哈尔滨医科大学附属第二医院黑龙江 哈尔滨 150081 
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中文摘要:
      低氧诱导因子2α是人体内重要的调控因子,主要存在于内皮细胞中。国内外的研究已经表明其在铁代谢、低氧适应、低氧性肺动脉高压形成、胎肺成熟、红细胞生成、肝脏生长等生理方面起重要作用。检索近10年国内外研究低氧诱导因子2α与骨关节炎进展关系的文献,发现其与骨关节炎的发生发展密切相关,主要通过直接或间接调控各种分解代谢因子,从而导致关节软骨的破坏和软骨基质的降解,因此,在关节软骨细胞的代谢中发挥重要的作用。随着医学研究的不断深入,低氧诱导因子2α在骨关节炎中的调控机制逐渐明了。本文就近年来与低氧诱导因子2α有关的上游或下游因子在骨关节炎中的调控作用作一综述,而这些因子已经被研究证明在骨关节炎中起到促进或抑制作用。例如基质金属蛋白酶-13、血管内皮细胞生长因子、烟酰胺磷酸核糖转移酶、骨桥蛋白、微小RNA-365和脂肪酸合酶等。从而进一步揭示低氧诱导因子2α作为核心调控因子在在骨关节炎的发生发展中的作用,为进一步理解骨关节炎的发病机制以及骨关节炎治疗提供一个新的途径。
英文摘要:
      Hypoxia-inducible factor 2α is an important regulator in human body and mainly present in endothelial cells. Studies in both China and overseas have shown that it plays an important role in iron metabolism, hypoxia adaptation, hypoxic pulmonary hypertension, fetal lung maturation, erythropoiesis, liver growth and other physiological aspects. It was found to be closely related to the occurrence and development of osteoarthritis, mainly through the direct or indirect regulation of various catabolic factors, resulting in the destruction of articular cartilage and cartilage matrix degradation, therefore, plays an important role in the metabolism of articular chondrocytes. With the advance of medical research, the regulation mechanism of hypoxia-inducible factor 2α in osteoarthritis has gradually become clear. In this paper, we reviewed recent studies on the regulation of upstream or downstream factors associated with hypoxia-inducible factor 2α in osteoarthritis, and these factors have been shown to promote or inhibit osteoarthritis. For example, matrix metalloproteinase-13, vascular endothelial growth factor, nicotinamide phosphoribosyltransferase, osteopontin, microRNA-365 and fatty acid synthase. Thus, the role of hypoxia-inducible factor 2α as a core regulator in the development of osteoarthritis is further revealed. This will provide a new way to further understand the pathogenesis of osteoarthritis and osteoarthritis treatment.
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