ArticleBMC pulmonary medicine2026
Clinical significance of LncRNA NORAD and its potential mechanism in chronic obstructive pulmonary disease.
Article in BMC pulmonary medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundChronic obstructive pulmonary disease (COPD) is a respiratory disease with complex causes; its pathogenesis remains unclear. This study explores the regulatory relationship between NORAD and miR-150-5p to provide novel insights for COPD treatment.
methodsSerum from 108 COPD patients and 94 healthy controls were collected. qPCR measured NORAD and miR-150-5p expression, while dual-luciferase assays verified their interaction. The clinical relevance of NORAD was analyzed using ROC, logistic, and Pearson methods. Human pulmonary microvascular endothelial cells (hPMECs) were treated with 5% cigarette smoke extract (CSE) for 36 h to establish a cell injury model. NORAD was silenced alone or co-inhibited with miR-150-5p in this model. Inflammatory and oxidative stress markers were measured by ELISA, and cell proliferation was assessed using the CCK-8 assay.
resultsCOPD patients exhibited significantly elevated serum NORAD level (P < 0.001), with higher levels in acute exacerbation than stable phases (P < 0.001). NORAD showed high diagnostic (AUC = 0.867, P < 0.001) and predictive value (OR = 3.271, P = 0.002) for COPD and was significantly correlated with lung function (P < 0.05). Serum NORAD was strongly negatively correlated with miR-150-5p (r = -0.749, P < 0.001), indicating a targeted regulatory relationship (P < 0.001). After CSE treatment, NORAD expression in hPMECs was significantly up-regulated (P < 0.001). NORAD knockdown reduced inflammation (P < 0.001), oxidative stress (P < 0.01), and reversed CSE-induced proliferation inhibition (P < 0.001). Co-inhibition of NORAD and miR-150-5p reversed the protective effect of NORAD knockdown (P < 0.05).
conclusionNORAD can regulate miR-150-5p, and both NORAD and miR-150-5p may serve as potential therapeutic targets for COPD, offering a promising strategy for modulating disease progression.
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