A selective inhibitor of mitofusin 1-βIIPKC association improves heart failure outcome in rats

Beta II protein kinase C (βIIPKC) activation contributes to heart failure. Here the authors show, in a rat model of myocardial infarction, that heart failure outcome can be improved by selectively inhibiting the interaction between βIIPKC and its downstream mitochondrial target Mitofusin-1, and that...

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Autores principales: Julio C. B. Ferreira, Juliane C. Campos, Nir Qvit, Xin Qi, Luiz H. M. Bozi, Luiz R. G. Bechara, Vanessa M. Lima, Bruno B. Queliconi, Marie-Helene Disatnik, Paulo M. M. Dourado, Alicia J. Kowaltowski, Daria Mochly-Rosen
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2019
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Acceso en línea:https://doaj.org/article/10da15e390414801950d6b6ca5915d4c
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Sumario:Beta II protein kinase C (βIIPKC) activation contributes to heart failure. Here the authors show, in a rat model of myocardial infarction, that heart failure outcome can be improved by selectively inhibiting the interaction between βIIPKC and its downstream mitochondrial target Mitofusin-1, and that this strategy is superior to global βIIPKC inhibition.