ArticleMolecular biology reports2026
miR-495-3p promotes chronic obstructive pulmonary disease by activating ferroptosis in lung epithelial cells through regulation of the ETS1/GPX4 axis.
Article in Molecular biology reports, 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
BACKGROUND AND
objectiveFerroptosis is a key pathogenic mechanism in chronic obstructive pulmonary disease (COPD). Bioinformatics analysis revealed that the expression of miR-495-3p is significantly upregulated in COPD, but its role in pulmonary epithelial cell ferroptosis has not been reported. This study aimed to investigate the regulatory function and molecular mechanism of miR-495-3p in the ferroptosis of pulmonary epithelial cells.
methodsLung tissue samples from nonsmokers, smokers, and smokers with COPD were collected. A cigarette smoke (CS)-induced COPD mouse model and a cigarette smoke extract (CSE)-induced BEAS-2B cell injury model were constructed. Pathological lung injury and collagen deposition were assessed via HE staining and Masson staining. Bronchoalveolar lavage fluid (BALF) total cell counts and BALF inflammatory cytokines were used to evaluate inflammation levels. Lactate dehydrogenase (LDH) activity was measured to assess cell death. Fe2+, GSH, MDA, and ROS levels were analyzed to evaluate ferroptosis. RT‒qPCR and western blotting were performed to detect the expression of key molecules. Dual-luciferase reporter assays were conducted to validate the targeting interaction between miR-495-3p and ETS1, and ChIP-qPCR was performed to detect ETS1 enrichment at the GPX4 promoter.
resultsmiR-495-3p was abnormally highly expressed in COPD. The knockdown of miR-495-3p expression significantly improved lung tissue injury, collagen deposition, and inflammatory responses in COPD mice. In vitro experiments revealed that miR-495-3p knockdown markedly reduced CSE-induced Fe2+, MDA, and ROS levels, restored the GSH content, and thereby inhibited cellular ferroptosis. Mechanistically, GPX4 expression was downregulated in the in vitro model, and inhibition of GPX4 expression attenuated the suppressive effect of miR-495-3p knockdown on ferroptosis. Further studies revealed that miR-495-3p downregulates GPX4 transcription by targeting ETS1. Knockdown of ETS1 or inhibition of GPX4 blocked the protective effect of miR-495-3p knockdown in COPD mice.
conclusionmiR-495-3p promotes ferroptosis in pulmonary epithelial cells by targeting ETS1 to downregulate GPX4 transcription, thereby driving COPD progression.
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