Research

 

CYP1 inhibition protects against anthracycline-induced cardiac toxicity

We identified a potent small molecule that protects against doxorubicin-induced heart dysfunction in zebrafish and mice. Using chemical and genetic approaches, we found that inhibition of cytochrome P450 family 1 enzymes is critical to the protective activity of these compounds.
 

 


 

Heme signaling and immune mechanisms in cardiomyopathy

We found that changes in the heme-binding protein hemopexin were associated with early cardiac toxicity in patients and in mice treated with anthracyclines. In mice, hemopexin protects against cardiac toxicity by modulating the monocyte/macrophage response and cardiac ferroptosis. In collaboration with the Kim lab, we defined the role of hemopexin and associated pathways in sickle cell cardiomyopathy. In collaboration with the Alcaide lab, we identified a role for cytotoxic T cells in doxorubicin-induced cardiac dysfunction.
 

 


 

Improving cardiac risk stratification in patients receiving anthracyclines

Our work has identified new clinical, blood, and ECG biomarkers associated with the development of early cardiac dysfunction and heart failure in patients treated with anthracyclines.

 

 


 

For a full list of publications from the Asnani lab, click here.