Cardiomyocytes, cardiac endothelial cells and fibroblasts contribute to anthracycline-induced cardiac injury through RAS-homologous small GTPases RAC1 and CDC42

• Autores principales: Pelin Kücük (Autor), Lena Abbey (Autor), Joachim Schmitt (Autor), Christian Henninger (Autor), Gerhard Fritz (Autor)
• Formato: Libro
• Publicado: Elsevier, 2024-05-01T00:00:00Z.
• Materias: article
• Acceso en línea: Connect to this object online.

The clinical use of the DNA damaging anticancer drug doxorubicin (DOX) is limited by irreversible cardiotoxicity, which depends on the cumulative dose. The RAS-homologous (RHO) small GTPase RAC1 contributes to DOX-induced DNA damage formation and cardiotoxicity. However, the pathophysiological relev...