Right Heart Failure in Mice Upon Pressure Overload Is Promoted by Mitochondrial Oxidative Stress

We sought to unravel pathomechanisms of the transition of maladaptive right ventricular (RV) remodeling to right heart failure (RHF) upon pressure overload. Exposure of C57BL/6J and C57BL/6N mice to pulmonary artery banding disclosed a tight relation of structural remodeling with afterload, but a di...

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Detalles Bibliográficos
Autores principales: Müller, Marion, Bischof, Cornelius, Kapries, Torben, Wollnitza, Sophie, Liechty, Chiara, Geißen, Simon, Schubert, Torben, Opacic, Dragan, Gerçek, Muhammed, Fortmeier, Vera, Dumitrescu, Daniel, Schlomann, Uwe, Sydykov, Akylbek, Petrovic, Aleksandar, Gnatzy-Feik, Leoni, Milting, Hendrik, Schermuly, Ralph T., Friedrichs, Kai, Rudolph, Volker, Klinke, Anna
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2022
Materias:
Original Research - Preclinical
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9357563/
https://www.ncbi.nlm.nih.gov/pubmed/35958691
http://dx.doi.org/10.1016/j.jacbts.2022.02.018
Descripción
Sumario:We sought to unravel pathomechanisms of the transition of maladaptive right ventricular (RV) remodeling to right heart failure (RHF) upon pressure overload. Exposure of C57BL/6J and C57BL/6N mice to pulmonary artery banding disclosed a tight relation of structural remodeling with afterload, but a dissociation from RV systolic function. Reduced release of mitochondrial reactive oxygen species in C57BL/6J mice prevented the development of RHF. In patients with left heart failure, increased oxidative damage in RV sections was associated with severely impaired RV function. In conclusion, reactive oxygen species are involved in the transition of maladaptive RV remodeling to RHF.

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