| http://purl.uniprot.org/citations/37884162 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/37884162 | http://www.w3.org/2000/01/rdf-schema#comment | "Myocardial infarction (MI) has been considered a leading cause of death worldwide. Relieving ischemia-reperfusion myocardial damage is one of the major roles in treating MI. Sevoflurane postconditioning provides myocardial protection, and this study probes the mechanism of sevoflurane-mediated protective effects. A hypoxia/reoxygenation (H/R) model was constructed in cardiomyocytes, which were pretreated with 2.4% sevoflurane. Alterations in SNHG10, miR-495-3p, and PTEN levels were determined, and gain- or loss-of functional assays were conducted to confirm the role of the SNHG10/miR-495-3p axis, which is potentially regulated by sevoflurane. Cell viability, oxidative stress, and inflammatory reactions were all evaluated. The results indicated that sevoflurane post-conditioning attenuated H/R-induced cardiomyocyte damage and reduced the SHNH10 level. SNHG10 overexpression reversed sevoflurane-mediated protective effects on cardiomyocytes. Moreover, SNHG10 targeted miR-495-3p and restrained its expression, while miR-495-3p targeted PTEN, suppressed PTEN levels, and promoted HIF-1α expression. miR-495-3p overexpression decreased SNHG10-mediated myocardial injury and enhanced HIF-1α levels. However, no additional protection was found when sevoflurane was administered to H/R-exposed cardiomyocytes following treatment with the HIF-1α inhibitor LW6. Overall, sevoflurane protects cardiomyocytes from H/R by modulating the SNHG10-miR-495-3p-PTEN-HIF-1α axis."xsd:string |
| http://purl.uniprot.org/citations/37884162 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.tiv.2023.105724"xsd:string |
| http://purl.uniprot.org/citations/37884162 | http://purl.uniprot.org/core/author | "Han C."xsd:string |
| http://purl.uniprot.org/citations/37884162 | http://purl.uniprot.org/core/author | "He J."xsd:string |
| http://purl.uniprot.org/citations/37884162 | http://purl.uniprot.org/core/author | "Zhang C."xsd:string |
| http://purl.uniprot.org/citations/37884162 | http://purl.uniprot.org/core/author | "Yu J."xsd:string |
| http://purl.uniprot.org/citations/37884162 | http://purl.uniprot.org/core/author | "Yang W."xsd:string |
| http://purl.uniprot.org/citations/37884162 | http://purl.uniprot.org/core/author | "Duan Y."xsd:string |
| http://purl.uniprot.org/citations/37884162 | http://purl.uniprot.org/core/author | "Hao W."xsd:string |
| http://purl.uniprot.org/citations/37884162 | http://purl.uniprot.org/core/date | "2024"xsd:gYear |
| http://purl.uniprot.org/citations/37884162 | http://purl.uniprot.org/core/name | "Toxicol In Vitro"xsd:string |
| http://purl.uniprot.org/citations/37884162 | http://purl.uniprot.org/core/pages | "105724"xsd:string |
| http://purl.uniprot.org/citations/37884162 | http://purl.uniprot.org/core/title | "The SNHG10-miR-495-3p-PTEN axis is involved in sevoflurane-mediated protective effects in cardiomyocytes against hypoxia/reoxygenation injury."xsd:string |
| http://purl.uniprot.org/citations/37884162 | http://purl.uniprot.org/core/volume | "94"xsd:string |
| http://purl.uniprot.org/citations/37884162 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/37884162 |
| http://purl.uniprot.org/citations/37884162 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/37884162 |
| http://purl.uniprot.org/uniprot/#_D0VY79-mappedCitation-37884162 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/37884162 |
| http://purl.uniprot.org/uniprot/#_A0A024QYR6-mappedCitation-37884162 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/37884162 |
| http://purl.uniprot.org/uniprot/#_A0A142FGX1-mappedCitation-37884162 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/37884162 |
| http://purl.uniprot.org/uniprot/#_A0A8V8TPK6-mappedCitation-37884162 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/37884162 |
| http://purl.uniprot.org/uniprot/#_A0A2P0XNP6-mappedCitation-37884162 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/37884162 |
| http://purl.uniprot.org/uniprot/#_A0A1V0DNR7-mappedCitation-37884162 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/37884162 |
| http://purl.uniprot.org/uniprot/#_A0A6G6A825-mappedCitation-37884162 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/37884162 |
| http://purl.uniprot.org/uniprot/#_F6KCZ4-mappedCitation-37884162 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/37884162 |