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Osteoprotegerin Disruption Attenuates HySu-Induced Pulmonary Hypertension Through Integrin αvβ3/FAK/AKT Pathway Suppression.
骨保护素破坏通过整合素 α v β3/FAK/AKT 通路抑制减轻 HySu 诱导的肺动脉高压。
biomarkers cell proliferation osteoprotegerin pulmonary hypertension pulmonary vascular smooth muscle cells
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摘要

BACKGROUND:Pulmonary arterial remodeling characterized by increased vascular smooth muscle proliferation is commonly seen in life-threatening disease, pulmonary arterial hypertension (PAH). Clinical studies have suggested a correlation between osteoprotegerin serum levels and PAH severity. Here, we aimed to invhestigate vascular osteoprotegerin expression and its effects on pulmonary arterial smooth muscle cell proliferation in vitro and in vivo, as well as examine the signal transduction pathways mediating its activity.
METHODS AND RESULTS:Serum osteoprotegerin levels were significantly elevated in patients with PAH and correlated with disease severity as determined by the World Health Organization (WHO) functional classifications and 6-minute walking distance tests. Similarly, increased osteoprotegerin expression was observed in the pulmonary arteries of hypoxia plus SU5416- and monocrotaline-induced PAH animal models. Moreover, osteoprotegerin disruption attenuated hypoxia plus SU5416-induced PAH progression by reducing pulmonary vascular remodeling, whereas lentiviral osteoprotegerin reconstitution exacerbated PAH by increasing pulmonary arterial smooth muscle cell proliferation. Furthermore, pathway analysis revealed that osteoprotegerin induced pulmonary arterial smooth muscle cell proliferation by interacting with integrin αvβ3 to elicit downstream focal adhesion kinase and AKT pathway activation.
CONCLUSIONS:Osteoprotegerin facilitates PAH pathogenesis by regulating pulmonary arterial smooth muscle cell proliferation, suggesting that it may be a potential biomarker and therapeutic target in this disease.

译文

背景: 以血管平滑肌增殖增加为特征的肺动脉重构常见于威胁生命的疾病 -- 肺动脉高压 (PAH)。临床研究表明骨保护素血清水平与 PAH 严重程度之间存在相关性。在此,我们旨在研究血管骨保护素的表达及其在体内外对肺动脉平滑肌细胞增殖的影响,并检测介导其活性的信号转导途径。
方法和结果: PAH 患者血清骨保护素水平显著升高,并与世界卫生组织 (WHO) 功能分类和 6 分钟步行距离测试确定的疾病严重程度相关。类似地,在缺氧加 SU5416 和野百合碱诱导的 PAH 动物模型的肺动脉中观察到骨保护素表达增加。此外,骨保护素破坏通过减少肺血管重构来减弱缺氧和 SU5416-induced 的 PAH 进展,而慢病毒骨保护素重建通过增加肺动脉平滑肌细胞增殖来加剧 PAH。此外,通路分析显示骨保护素通过与整合素 α v β3 相互作用引起下游粘着斑激酶和 AKT 通路激活,从而诱导肺动脉平滑肌细胞增殖。
结论: 骨保护素通过调节肺动脉平滑肌细胞增殖促进 PAH 发病,提示其可能是该疾病的潜在生物标志物和治疗靶点。

osteoprotegerin

骨科 骨质疏松 药物
概述  :  

骨保护素是由成骨细胞分泌的一种无跨膜结构的可溶性糖蛋白,参与骨代谢的一种细胞因子,在骨代谢的研究中具有里程碑的意义。因其同时参与影响血管钙化和动脉硬化的过程,被认为是动脉粥样硬化的独立危险因子。OPG与骨代谢、心血管系统、免疫系统等有着重要的联系,在骨质疏松症、类风湿关节炎、骨髓瘤、冠心病、Paget病等多种疾病中都发现OPG mRNA水平异常。   作用机制 骨保护素是近年来骨质疏松症防治领域最重要的发现。OPG由成骨

osteoprotegerin

释义   骨保护素;护骨素

短语   osteoprotegerin ligand 骨保护素配体  

osteoprotegerin biomechanics 骨保护素生物力学

osteoprotegerin system 骨保护素系统

osteoprotegerin gene 护骨素基因

例句   Serum osteoprotegerin level and bone density of the patients were measured before the treatment, after treatment for 6 months and 12 months respectively. 分别于治疗前、治疗6个月、治疗12个月时测定患者的血清骨保护素水平和骨密度。

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