Knockdown of Mtfp1 can minimize doxorubicin cardiotoxicity by inhibiting Dnm1l‐mediated mitochondrial fission

The long‐term usage of doxorubicin (DOX) is largely limited due to the development of severe cardiomyopathy. Many studies indicate that DOX‐induced cardiac injury is related to reactive oxygen species generation and ultimate activation of apoptosis. The role of novel mitochondrial fission protein 1...

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Detalles Bibliográficos
Autores principales: Aung, Lynn H. H., Li, Ruibei, Prabhakar, Bellur S., Li, Peifeng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2017
Materias:
Original Articles
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5706585/
https://www.ncbi.nlm.nih.gov/pubmed/28643438
http://dx.doi.org/10.1111/jcmm.13250

Internet

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5706585/
https://www.ncbi.nlm.nih.gov/pubmed/28643438
http://dx.doi.org/10.1111/jcmm.13250

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