Publication: LncRNA TUG1 aggravates cardiomyocyte apoptosis and myocardial ischemia/reperfusion injury
| dc.contributor.author | Fu, Dongliang | |
| dc.contributor.author | Gao, Tong | |
| dc.contributor.author | Liu, Mengru | |
| dc.contributor.author | Li, Chunyan | |
| dc.contributor.author | Li, Haiwei | |
| dc.contributor.author | Jiang, Hong | |
| dc.contributor.author | Li, Xianlun | |
| dc.date.accessioned | 2023-02-02T11:21:01Z | |
| dc.date.available | 2023-02-02T11:21:01Z | |
| dc.date.issued | 2021 | |
| dc.description.abstract | Cardiomyocyte apoptosis is a fundamental pathogenic factor leading to myocardial ischemia/ reperfusion (MI/R) injury. The long non-coding RNA (lncRNA) TUG1 regulates apoptosis in various cell types. We report here that TUG1 expression is induced in mouse heart following MI/R injury as well as in cardiomyocytes subjected to simulated ischemia/ reperfusion (SI/R) in vitro. Clinically, TUG1 expression is also elevated in plasma from patients with acute myocardial infarction (AMI), which implies its potential application as a disease biomarker. Functionally, TUG1 overexpression promotes, and its knockdown reduces SI/R-induced lactate dehydrogenase (LDH) release and caspase-3 activity in cardiomyocytes in vitro, illustrating that TUG1 exacerbates SI/R-induced apoptosis. Furthermore, in vivo, TUG1 aggravates MI/R injury in a mouse model, and subsequent observations show concurrent increased apoptosis of cardiomyocytes. Hence, this study unveils a clinical relevance and functional role of TUG1 in MI/R injury, and also implicates that targeting TUG1 m | es |
| dc.format | application/pdf | es |
| dc.format.extent | 12 | es |
| dc.identifier.citation | Histology and Histopathology Vol. 36, nº12 (2021) | |
| dc.identifier.doi | https://doi.org/10.14670/HH-18-381 | |
| dc.identifier.issn | 0213-3911 | |
| dc.identifier.issn | 1699-5848 | |
| dc.identifier.uri | http://hdl.handle.net/10201/128105 | |
| dc.language | eng | es |
| dc.publisher | Universidad de Murcia, Departamento de Biologia Celular e Histiologia | es |
| dc.relation | Sin financiación externa a la Universidad | es |
| dc.rights | info:eu-repo/semantics/openAccess | es |
| dc.rights | Attribution-NonCommercial-NoDerivatives 4.0 Internacional | * |
| dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | * |
| dc.subject | LncRNA | es |
| dc.subject | TUG1 | es |
| dc.subject | Myocardial ischemia | es |
| dc.subject | reperfusion injury | es |
| dc.subject | Apoptosis | es |
| dc.subject.other | CDU::6 - Ciencias aplicadas::61 - Medicina::616 - PatologÃa. Medicina clÃnica. OncologÃa | es |
| dc.title | LncRNA TUG1 aggravates cardiomyocyte apoptosis and myocardial ischemia/reperfusion injury | es |
| dc.type | info:eu-repo/semantics/article | es |
| dspace.entity.type | Publication | es |
Este Ãtem está sujeto a una licencia Creative Commons. http://creativecommons.org/licenses/by-nc-nd/4.0/