Mostrar el registro sencillo del ítem
Cardiac remodeling and arrhythmogenesis are ameliorated by administration of Cx43 mimetic peptide Gap27 in heart failure rats
dc.contributor.author | Lucero C.M. | |
dc.contributor.author | Andrade D.C. | |
dc.contributor.author | Toledo C. | |
dc.contributor.author | Díaz H.S. | |
dc.contributor.author | Pereyra K.V. | |
dc.contributor.author | Diaz-Jara E. | |
dc.contributor.author | Schwarz K.G. | |
dc.contributor.author | Marcus N.J. | |
dc.contributor.author | Retamal M.A. | |
dc.contributor.author | Quintanilla R.A. | |
dc.contributor.author | Del Rio R. | |
dc.date.accessioned | 2020-09-02T22:21:49Z | |
dc.date.available | 2020-09-02T22:21:49Z | |
dc.date.issued | 2020 | |
dc.identifier | 10.1038/s41598-020-63336-6 | |
dc.identifier.citation | 10, 1, - | |
dc.identifier.issn | 20452322 | |
dc.identifier.uri | https://hdl.handle.net/20.500.12728/5117 | |
dc.description | Alterations in connexins and specifically in 43 isoform (Cx43) in the heart have been associated with a high incidence of arrhythmogenesis and sudden death in several cardiac diseases. We propose to determine salutary effect of Cx43 mimetic peptide Gap27 in the progression of heart failure. High-output heart failure was induced by volume overload using the arterio-venous fistula model (AV-Shunt) in adult male rats. Four weeks after AV-Shunt surgery, the Cx43 mimetic peptide Gap27 or scrambled peptide, were administered via osmotic minipumps (AV-ShuntGap27 or AV-ShuntScr) for 4 weeks. Cardiac volumes, arrhythmias, function and remodeling were determined at 8 weeks after AV-Shunt surgeries. At 8th week, AV-ShuntGap27 showed a marked decrease in the progression of cardiac deterioration and showed a significant improvement in cardiac functions measured by intraventricular pressure-volume loops. Furthermore, AV-ShuntGap27 showed less cardiac arrhythmogenesis and cardiac hypertrophy index compared to AV-ShuntScr. Gap27 treatment results in no change Cx43 expression in the heart of AV-Shunt rats. Our results strongly suggest that Cx43 play a pivotal role in the progression of cardiac dysfunction and arrhythmogenesis in high-output heart failure; furthermore, support the use of Cx43 mimetic peptide Gap27 as an effective therapeutic tool to reduce the progression of cardiac dysfunction in high-output heart failure. © 2020, The Author(s). | |
dc.language.iso | en | |
dc.publisher | Nature Research | |
dc.title | Cardiac remodeling and arrhythmogenesis are ameliorated by administration of Cx43 mimetic peptide Gap27 in heart failure rats | |
dc.type | Article |