Differential Transcriptomic Signatures of Small Airway Cell Cultures Derived from IPF and COVID-19-Induced Exacerbation of Interstitial Lung Disease.
Differential Transcriptomic Signatures of Small Airway Cell Cultures Derived from IPF and COVID-19-Induced Exacerbation of Interstitial Lung Disease.
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特发性肺纤维化（IPF）是一种病理状况，其中肺损伤促使瘢痕组织沉积，最终导致肺功能下降。现有研究表明，感染COVID-19后，IPF患者的临床预后显著恶化。这项研究采用批量RNA测序方法来描述来自IPF和COVID后纤维化患者的小气道细胞培养物的转录组学特征。差异基因表达分析揭示了IPF细胞培养物中与微管组装和干扰素信号传导相关的途径的活化增强。相反，COVID后纤维化细胞培养物表现出独特的特征，包括与细胞外基质重塑、免疫系统反应和TGF-β1信号传导相关的通路的上调。值得注意的是，与非IPF对照和COVID后纤维化样品相比，源自IPF患者的细胞培养物中BMP信号传导水平升高。这些发现强调了IPF和COVID后纤维化之间的分子差异，特别是在与每种疾病相关的信号通路的背景下。更好地了解潜在的分子机制有望为这些疾病的未来干预措施确定潜在的治疗靶点。
Idiopathic pulmonary fibrosis (IPF) is a pathological condition wherein lung injury precipitates the deposition of scar tissue, ultimately leading to a decline in pulmonary function. Existing research indicates a notable exacerbation in the clinical prognosis of IPF patients following infection with COVID-19. This investigation employed bulk RNA-sequencing methodologies to describe the transcriptomic profiles of small airway cell cultures derived from IPF and post-COVID fibrosis patients. Differential gene expression analysis unveiled heightened activation of pathways associated with microtubule assembly and interferon signaling in IPF cell cultures. Conversely, post-COVID fibrosis cell cultures exhibited distinctive characteristics, including the upregulation of pathways linked to extracellular matrix remodeling, immune system response, and TGF-β1 signaling. Notably, BMP signaling levels were elevated in cell cultures derived from IPF patients compared to non-IPF control and post-COVID fibrosis samples. These findings underscore the molecular distinctions between IPF and post-COVID fibrosis, particularly in the context of signaling pathways associated with each condition. A better understanding of the underlying molecular mechanisms holds the promise of identifying potential therapeutic targets for future interventions in these diseases.
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影响因子：
14.9
作者：
Gene Ontology Consortium
通讯作者：
Gene Ontology Consortium
影响因子：
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作者：
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Martini C
DOI：
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发表时间：
2012-03-01
影响因子：
24.7
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DOI：
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2014-01-15
影响因子：
24.7
作者：
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DOI：
10.3390/medsci6040110
发表时间：
2018-11-29
期刊：
Medical sciences (Basel, Switzerland)
影响因子：
--
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Soriano JB