Key result
miR-138-5p overexpression inhibits aortic valve cell calcification by targeting SLC39A14 and activating Nrf2 signaling.
Why the study?
This study explored the role of miR-138-5p in calcific aortic valve disease, focusing on its regulation of osteogenic differentiation in human aortic valve interstitial cells and underlying mechanisms.
Population
Aortic valve tissues from CAVD patients and controls, and cultured hAVICs
Comparison
miR-138-5p mimics or inhibitors, SLC39A14 overexpression, and ML385 vs controls
Design
In vitro and ex vivo preclinical experimental study
Authors
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Hypothesis-generating for miR-138-5p in CAVD; leaves open clinical relevance pending in vivo validation.
miR-138-5p inhibits calcification of human aortic valve interstitial cells by targeting SLC39A14 and activating the Nrf2 pathway, identifying a potential therapeutic target for calcific aortic valve disease.
Yan et al. (2026) studied Calcific aortic valve disease (CAVD). miR-138-5p overexpression vs. Controls was evaluated on Calcification (ALP activity, nodule formation, and osteogenic marker expression). Overexpression of miR-138-5p inhibited calcification in human aortic valve interstitial cells by targeting SLC39A14 and activating the Nrf2 signaling pathway.
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