ArticleApplied biochemistry and biotechnology2025
Sevoflurane Alleviates Myocardial Ischemia/Reperfusion Injury Via Regulating TRIM65-Mediated Ubiquitination Modification of ALOX5.
Article in Applied biochemistry and biotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Ubiquitination-dependent regulation of ferroptosis in ischemic heart and brain.Redox biology · 2026Review
- ATP-P2X7R-NLRP3 Axis as a Unifying Mechanism of ATP-Induced Cell Death in Degenerative Bone and Cardiovascular Diseases.Journal of inflammation research · 2026Review
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4 authors.
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Abstract
Background As a commonly used anesthetic in clinical practice, sevoflurane (Sevo) has been found to have a certain protective effect on myocardial ischemia/reperfusion (MI/R) injury. However, the underlying molecular mechanisms deserve further elucidation. Methods Human cardiomyocytes were induced by hypoxia/reoxygenation (H/R), and MI/R rat model was established by ligation of left coronary artery. Cell viability and apoptosis were tested using CCK8 assay and flow cytometry. Inflammatory factors and ferroptosis-related markers were tested by corresponding kit. The levels of ALOX5, ferroptosis-related markers, and tripartite motif 65 (TRIM65) were determined by qRT-PCR or western blot. The interaction between TRIM65 and ALOX5 was evaluated by Co-IP assay. Results Sevo repressed H/R-induced cardiomyocyte apoptosis, inflammation, and ferroptosis. Sevo reduced the ALOX5 protein level, and ALOX5 overexpression reversed the inhibitory effects of Sevo on H/R-induced cardiomyocyte injury. E3 ubiquitin ligase TRIM65 could decrease ALOX5 protein stability by promoting its ubiquitination level. TRIM65 inhibited H/R-induced cardiomyocyte apoptosis, inflammation, and ferroptosis by downregulating ALOX5. Furthermore, TRIM65 knockdown reversed the protective effects of Sevo on H/R-induced cardiomyocyte injury. Additionally, Sevo alleviated MI/R injury in rat models by activating TRIM65-mediated ubiquitination of ALOX5. Conclusion Sevo restrained H/R-induced cardiomyocyte apoptosis, inflammation, and ferroptosis to alleviate MI/R injury, which might be associated with the TRIM65/ALOX5 axis.
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