ArticleJournal of biochemical and molecular toxicology2026
miR-138-5p Inhibits Aortic Valve Interstitial by Targeting SLC39A14 and Activating Nrf2 Signaling.
Article in Journal of biochemical and molecular toxicology, 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
This study explored the role of miR-138-5p in calcific aortic valve disease (CAVD), focusing on its regulation of osteogenic differentiation in human aortic valve interstitial cells (hAVICs) and underlying mechanisms. Aortic valve tissues from CAVD patients and controls were analyzed for miR-138-5p expression using qRT-PCR. hAVICs were cultured in osteogenic medium (OM) and transfected with miR-138-5p mimics or inhibitors. Calcification was evaluated via ALP and Alizarin Red staining. Western blot assessed osteogenic markers (RUNX2, ALP, OPN, BMP-2). Dual-luciferase assays confirmed miR-138-5p targeting of SLC39A14. The role of SLC39A14 and the Nrf2 pathway was examined through overexpression experiments and Western blot for Nrf2, HO-1, and NQO1. ML385 was used to inhibit Nrf2. miR-138-5p was significantly downregulated in CAVD tissues and OM-induced hAVICs. Overexpression of miR-138-5p inhibited calcification, reducing ALP activity, nodule formation, and osteogenic marker expression. Inhibition of miR-138-5p promoted calcification. SLC39A14, upregulated in CAVD, was validated as a direct target of miR-138-5p. Its overexpression promoted calcification, which was reversed by co-transfection with miR-138-5p. Mechanistically, miR-138-5p was associated with activation of the Nrf2 pathway, as evidenced by increased Nrf2 nuclear translocation and HO-1/NQO1 expression, whereas SLC39A14 overexpression showed the opposite effect. Nrf2 inhibition with ML385 diminished the anti-calcific effect of miR-138-5p. miR-138-5p inhibits hAVIC calcification, at least in part through regulation of SLC39A14 and the Nrf2 pathway, highlighting a potentially important regulatory mechanism in CAVD and a candidate therapeutic target for valve calcification.
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