Wnt10b protects cardiomyocytes against doxorubicin-induced cell death via MAPK modulation.

ABSTRACT:

Background

Doxorubicin, an anthracycline chemotherapeutic known to incur heart damage, decreases heart function in up to 11% of patients. Recent investigations have implicated the Wnt signaling cascade as a key modulator of cardiac tissue repair after myocardial infarction. Wnt upregulation in murine models resulted in stimulation of angiogenesis and suppression of fibrosis after ischemic insult. However, the molecular mechanisms of Wnt in mitigating doxorubicin-induced cardiac insult require further investigation. Identifying cardioprotective mechanisms of Wnt is imperative to reducing debilitating cardiovascular adverse events in oncologic patients undergoing treatment.

Methods

Exposing human cardiomyocyte AC16 cells to varying concentrations of Wnt10b and DOX, we observed

SUBMITTER: Chen L 

PROVIDER: S-EPMC10586692 | biostudies-literature | 2023

REPOSITORIES: biostudies-literature