Cardiomyocyte GSDME Drives Doxorubicin-Induced Cardiotoxicity by Targeting the CCL2-CCR2 Axis.

ABSTRACT: The use of doxorubicin (DOX), a wide-spectrum antineoplastic drug, is largely limited in clinical practice because of the less than satisfactory strategies available for the prevention and treatment of doxorubicin-induced cardiotoxicity (DIC). Although gasdermin E (GSDME) has been linked to the development of several cardiovascular diseases, the role of GSDME in DIC has not been thoroughly investigated. Here, we aimed to explore the role of GSDME in the development of DIC and develop efficient and feasible targets for managing DIC. We found that GSDME was upregulated in both DOX-treated murine hearts and isolated adult mouse cardiomyocytes. Conditional Gsdme knockout in cardiomyocytes, but not myeloid cells, attenuated DOX-induced cardiac remodeling, cardiac malfunction, and cardiac

SUBMITTER: Xue J 

PROVIDER: S-EPMC12594575 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature