{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,7]],"date-time":"2026-07-07T22:57:30Z","timestamp":1783465050127,"version":"3.55.0"},"reference-count":39,"publisher":"Georg Thieme Verlag KG","issue":"05","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Thorac Cardiovasc Surg"],"published-print":{"date-parts":[[2025,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Ferroptosis is emerging as a critical pathway in ischemia\/reperfusion (I\/R) injury, contributing to compromised cardiac function and predisposing individuals to sepsis and myocardial failure. The study investigates the underlying mechanism of dexmedetomidine (DEX) in hypoxia\/reoxygenation (H\/R)-induced ferroptosis in cardiomyocytes, aiming to identify novel targets for myocardial I\/R injury treatment.<\/jats:p><jats:p>H9C2 cells were subjected to H\/R and treated with varying concentrations of DEX. Additionally, H9C2 cells were transfected with miR-141-3p inhibitor followed by H\/R treatment. Levels of miR-141-3p, long noncoding RNA (lncRNA) taurine upregulated 1 (TUG1), Fe2+, glutathione (GSH), and malondialdehyde were assessed. Reactive oxygen species (ROS) generation was measured via fluorescent labeling. Expression of ferroptosis-related proteins glutathione peroxidase 4 (GPX4) and acyl-CoA synthetase long-chain family member 4 (ACSL4) was determined using Western blot. The interaction between miR-141-3p and lncRNA TUG1 was evaluated through RNA pull-down assay and dual-luciferase reporter gene assays. The stability of lncRNA TUG1 was assessed using actinomycin D.<\/jats:p><jats:p>DEX ameliorated H\/R-induced cardiomyocyte injury and elevated miR-141-3p expression in cardiomyocytes. DEX treatment increased cell viability, Fe2+, and ROS levels while decreasing ACSL4 protein expression. Furthermore, DEX upregulated GSH and GPX4 protein levels. miR-141-3p targeted lncRNA TUG1, reducing its stability and overall expression. Inhibition of miR-141-3p or overexpression of lncRNA TUG1 partially reversed the inhibitory effect of DEX on H\/R-induced ferroptosis in cardiomyocytes.<\/jats:p><jats:p>DEX mitigated H\/R-induced ferroptosis in cardiomyocytes by upregulating miR-141-3p expression and downregulating lncRNA TUG1 expression, unveiling a potential therapeutic strategy for myocardial I\/R injury.<\/jats:p>","DOI":"10.1055\/s-0044-1787691","type":"journal-article","created":{"date-parts":[[2024,6,18]],"date-time":"2024-06-18T19:01:30Z","timestamp":1718737290000},"page":"410-417","source":"Crossref","is-referenced-by-count":5,"title":["DEX Inhibits H\/R-induced Cardiomyocyte Ferroptosis by the miR-141-3p\/lncRNA TUG1 Axis"],"prefix":"10.1055","volume":"73","author":[{"ORCID":"https:\/\/orcid.org\/0009-0009-2214-9205","authenticated-orcid":false,"given":"Mei","family":"Zhu","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology, Taizhou People's Hospital Affiliated to Nanjing Medical 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