Scholarlink

<p>Chronic Obstructive Pulmonary Disease (COPD) is a complex respiratory disorder characterized by chronic inflammation and irreversible airflow limitation, primarily resulting from long-term exposure to harmful particles or gases, primarily from smoking. Dysregulation of microRNAs (miRNAs) contributes to COPD pathogenesis, influencing inflammation, airway and vascular remodeling, and oxidative stress responses. The study evaluated the expression of selected miRNAs involved in PI3K/AKT and focal adhesion pathways as potential COPD biomarkers. Lung tissue and peripheral blood mononuclear cells (PBMCs) were collected from COPD patients and healthy controls. RT-qPCR and TaqMan™ MicroRNA Assay (Thermo Fisher Scientific) were used to quantify expression levels of miR-218-5p, miR-126-3p, miR-200a-3p, miR-18a-5p, miR-29a-3p, miR-34a-5p, miR-155-5p, miR-141-3p, miR-15b-5p, miR-379-5p, miR-150-5p, miR-570-3p. Nine miRNAs were differentially expressed in PBMCs, and six in lung tissue of COPD patients, with four miRNAs (miR-18a-5p, miR-34a-5p, miR-126-3p, and miR-218-5p) altered in both. Multivariate models constructed using multiple regression demonstrated strong discrimination of COPD patients from controls, with AUC of 0.899 (combined assessment of miR-218-5p, miR-126-3p, miR-150-5p, and miR-29a-3p expression in PBMCs) and 0.965 (combined assessment of miR-218-5p, miR-141-3p, miR-379-5p, and miR-18a-5p expression in lung tissue). In silico pathway enrichment analysis linked the differentially expressed miRNAs to PI3K/AKT signaling, protein processing in the endoplasmic reticulum, focal adhesion, apoptosis, autophagy, and cellular senescence. The identified miRNAs are promising COPD biomarkers reflecting key pathogenic processes. Further validation in independent cohorts and functional studies are needed to confirm their clinical utility and to clarify their roles in disease progression.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

The Role of MicroRNAs Implicated in the Regulation of PI3K/AKT and Focal Adhesion Signaling Pathways in Chronic Obstructive Pulmonary Disease

  • 期刊论文

  • 发表日期：

    2026年4月7日

查看全文
  • Gulnaz Korytina,
  • Vitaly Markelov,
  • Timur Nasibullin,
  • Yanina Timasheva,
  • Leysan Akhmadishina,
  • Yulia Aznabaeva,
  • Irshat Gibadullin,
  • Olga Kochetova,
  • Naufal Zagidullin

摘要

Chronic Obstructive Pulmonary Disease (COPD) is a complex respiratory disorder characterized by chronic inflammation and irreversible airflow limitation, primarily resulting from long-term exposure to harmful particles or gases, primarily from smoking. Dysregulation of microRNAs (miRNAs) contributes to COPD pathogenesis, influencing inflammation, airway and vascular remodeling, and oxidative stress responses. The study evaluated the expression of selected miRNAs involved in PI3K/AKT and focal adhesion pathways as potential COPD biomarkers. Lung tissue and peripheral blood mononuclear cells (PBMCs) were collected from COPD patients and healthy controls. RT-qPCR and TaqMan™ MicroRNA Assay (Thermo Fisher Scientific) were used to quantify expression levels of miR-218-5p, miR-126-3p, miR-200a-3p, miR-18a-5p, miR-29a-3p, miR-34a-5p, miR-155-5p, miR-141-3p, miR-15b-5p, miR-379-5p, miR-150-5p, miR-570-3p. Nine miRNAs were differentially expressed in PBMCs, and six in lung tissue of COPD patients, with four miRNAs (miR-18a-5p, miR-34a-5p, miR-126-3p, and miR-218-5p) altered in both. Multivariate models constructed using multiple regression demonstrated strong discrimination of COPD patients from controls, with AUC of 0.899 (combined assessment of miR-218-5p, miR-126-3p, miR-150-5p, and miR-29a-3p expression in PBMCs) and 0.965 (combined assessment of miR-218-5p, miR-141-3p, miR-379-5p, and miR-18a-5p expression in lung tissue). In silico pathway enrichment analysis linked the differentially expressed miRNAs to PI3K/AKT signaling, protein processing in the endoplasmic reticulum, focal adhesion, apoptosis, autophagy, and cellular senescence. The identified miRNAs are promising COPD biomarkers reflecting key pathogenic processes. Further validation in independent cohorts and functional studies are needed to confirm their clinical utility and to clarify their roles in disease progression.