Approved Research

AT1R as the core bond between AML and CVD

Lay summary

Acute Myeloid Leukemia (AML) and Cardiovascular Disease (CVD) have significant clinical association. To determine if there is a shared target between AML and CVD, we will analyze the genetic pattern between AML and CVD. We expect angiotensin 2 receptor type 1 (AT1R) to be the core bond between AML and CVD. AT1R has been implicated in various CVDs, such as hypertension, coronary artery disease and stroke. However, AT1R's role in AML has not been well studied. In our preliminary studies, we found AT1R expression was highly increased on the cell surface of human AML cells compared with healthy control, and genetic mouse models showed a delay of leukemia development after AT1R knockout.

Our aim is to identify shared targets between AML and CVD and evaluate AT1R's role in AML within 36 months.

These studies should provide a strong rationale in support of AT1R inhibition as a potential treatment for human AML. Moreover, standard chemotherapy regimens used for AML treatment are associated with significant side effects including cardiotoxicity. Studies have shown that angiotensin signaling is important for chemotherapy-induced cardiotoxicity. AT1R inhibition may also reduce cardiotoxicities in AML patients undergoing chemotherapy.