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Astaxanthin attenuates pulmonary fibrosis through lncITPF and mitochondria-mediated signal pathways.
Journal of Cellular and Molecular Medicine ( IF 4.3 ) Pub Date : 2020-08-19 , DOI: 10.1111/jcmm.15477
Hongbin Chen 1 , Jing Wang 1 , Rongrong Li 2 , Changjun Lv 1, 2 , Pan Xu 2 , Youlei Wang 1 , Xiaodong Song 1, 2 , Jinjin Zhang 1, 2
Affiliation  

Pulmonary fibrosis is a chronic interstitial lung disease characterized by pulmonary epithelial injury, fibroblast activation, extracellular matrix deposition, and tissue structure destruction. However, an effective drug treatment remains unavailable. Therefore, studying the mechanism of pulmonary fibrogenesis and finding effective drugs have become important problems in the field of respiratory diseases. Pulmonary fibrosis is typically characterized by activated fibroblast proliferation and migration. Hence, abnormality in activated fibroblast proliferation and migration is a major concern for treating pulmonary fibrosis. Long noncoding RNA (lncRNA) is an enigmatic subclass of ncRNA that regulates various fundamental biological processes and participates in disease occurrence and development. However, studies on lncRNA as the therapeutic target of drug action are rarely reported. Our group first identified differentially expressed lncRNAs and revealed that lncITPF is a highly upregulated lncRNA in lung fibrosis. In particular, lncITPF is detected in the blood of patients with idiopathic pulmonary fibrosis. Clinical analysis shows that lncITPF is positively correlated with the degree of fibrosis. The receiver operating characteristic (ROC) curve indicates that the specificity and sensitivity values are 95.0 and 64.3, respectively. The area under the ROC curve is 0.804, indicating that lncITPF can be a diagnostic biomarker for IPF. However, whether lncITPF is effective as a therapeutic target of drug action against pulmonary fibrosis remains unclear. In this study, lncITPF acting as the therapeutic target of astaxanthin was explored in depth. The findings elucidated that astaxanthin blocks the activated fibroblast proliferation and migration through lncITPF and mitochondria‐mediated signal pathways to alleviate pulmonary fibrogenesis.

中文翻译:

虾青素通过lncITPF和线粒体介导的信号通路减轻肺纤维化。

肺纤维化是一种慢性间质性肺疾病,其特征是肺上皮损伤,成纤维细胞活化,细胞外基质沉积和组织结构破坏。但是,仍然没有有效的药物治疗方法。因此,研究肺纤维化的机理并寻找有效的药物已成为呼吸系统疾病领域的重要问题。肺纤维化的典型特征是活化的成纤维细胞增殖和迁移。因此,活化成纤维细胞增殖和迁移的异常是治疗肺纤维化的主要问题。长非编码RNA(lncRNA)是ncRNA的一个神秘子类,它调节各种基本的生物学过程并参与疾病的发生和发展。然而,关于lncRNA作为药物作用的治疗靶标的研究很少报道。我们的小组首先鉴定了差异表达的lncRNA,并发现lncITPF是肺纤维化中高度上调的lncRNA。特别地,在患有特发性肺纤维化的患者的血液中检测到lncITPF。临床分析表明,lncITPF与纤维化程度呈正相关。接收器工作特性(ROC)曲线表明特异性和灵敏度值分别为95.0和64.3。ROC曲线下的面积为0.804,表明lncITPF可以作为IPF的诊断生物标志物。然而,仍不清楚lncITPF是否有效作为针对肺纤维化的药物作用的治疗靶标。在这项研究中,深入研究了作为虾青素治疗靶标的lncITPF。
更新日期:2020-09-28
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