New insights into the molecular mechanisms underlying the development of doxorubicin-induced cardiomyopathy: the role of MST1 activation
| Componente | Categoria |
|---|---|
| Giuseppe Cimino | Componenti strutturati del gruppo di ricerca / Structured participants in the research project |
| Clara Nervi | Componenti strutturati del gruppo di ricerca / Structured participants in the research project |
| Leonardo Schirone | Dottorando/Assegnista/Specializzando componente non strutturato del gruppo di ricerca / PhD/Assegnista/Specializzando member non structured of the research group |
| Cristina Nocella | Componenti strutturati del gruppo di ricerca / Structured participants in the research project |
| Luciano De Biase | Componenti strutturati del gruppo di ricerca / Structured participants in the research project |
Doxorubicin (DOX) is a powerful chemotherapeutic agent that is largely used in the clinical practice for cancer treatment. Unfortunately, nearly 30% of DOX-treated patients develop heart failure, which represents the first noncancer-related cause of death in these patients. The molecular mechanisms underlying DOX-induced cardiotoxicity remain largely unclear. Our preliminary results indicate that the kinase MST1 is involved in DOX-induced cardiomyopathy. MST1 is a major component of the Hippo pathway, which negatively regulates cell survival and growth and was previously shown to contribute to myocardial injury in response to stress. We will study the phenotype of mice with cardiomyocyte-specific MST1 gene deletion treated with DOX. We will elucidate the molecular mechanisms through which MST1 contributes to DOX-induced cardiomyopathy, with a focus on the involvement of SIRT3.