Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 황금숙 | * |
dc.date.accessioned | 2017-11-01T05:01:59Z | - |
dc.date.available | 2017-11-01T05:01:59Z | - |
dc.date.issued | 2017 | * |
dc.identifier.issn | 2045-2322 | * |
dc.identifier.other | OAK-21259 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/239076 | - |
dc.description.abstract | Inflammation is a common cause of cardiac arrhythmia. Angiotensin II (Ang II) is a major contributing factor in the pathogenesis of cardiac inflammation; however, its underlying molecular mechanism remains unclear. Here, we explored the effect of Ang II on inflammatory mechanisms and oxidative stress using HL-1 atrial myocytes. We showed that Ang II activated c-Jun N-terminal kinase (JNK) phosphorylation and other inflammatory markers, such as transforming growth factor-β1 (TGF-β1) and tumor necrosis factor-α (TNF-α). Ang II decreased oxygen consumption rate, which resulted in reactive oxygen species (ROS) generation and inhibition of ROS blocked Ang II-mediated JNK phosphorylation and TGF-β1 induction. Ang II induced the expression of its specific receptor, AT1R. Ang II-induced intracellular calcium production associated with Ang II-mediated signalling pathways. In addition, the generated ROS and calcium stimulated AMPK phosphorylation. Inhibiting AMPK blocked Ang II-mediated JNK and TGF-β signalling pathways. Ang II concentration, along with TGF-β1 and tumor necrosis factor-α levels, was slightly increased in plasma of patients with atrial fibrillation. Taken together, these results suggest that Ang II induces inflammation mechanisms through an AMPK-related signalling pathway. Our results provide new molecular targets for the development of therapeutics for inflammation-related conditions, such as atrial fibrillation. © 2017 The Author(s). | * |
dc.language | English | * |
dc.publisher | Nature Publishing Group | * |
dc.title | Angiotensin II affects inflammation mechanisms via AMPK-related signalling pathways in HL-1 atrial myocytes | * |
dc.type | Article | * |
dc.relation.issue | 1 | * |
dc.relation.volume | 7 | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.journaltitle | Scientific Reports | * |
dc.identifier.doi | 10.1038/s41598-017-09675-3 | * |
dc.identifier.wosid | WOS:000408997700027 | * |
dc.identifier.scopusid | 2-s2.0-85028816615 | * |
dc.author.google | Kim N. | * |
dc.author.google | Jung Y. | * |
dc.author.google | Nam M. | * |
dc.author.google | Sun Kang M. | * |
dc.author.google | Lee M.K. | * |
dc.author.google | Cho Y. | * |
dc.author.google | Choi E.-K. | * |
dc.author.google | Hwang G.-S. | * |
dc.author.google | Soo Kim H. | * |
dc.contributor.scopusid | 황금숙(7202676099) | * |
dc.date.modifydate | 20240222154747 | * |