A new study by Washington State University researchers suggests that a protein called CDK2 plays a critical role in heart damage caused by doxorubicin, a commonly used chemotherapy drug.
A new study by Washington State University researchers suggests that a protein called CDK2 plays a critical role in heart damage caused by doxorubicin, a commonly used chemotherapy drug.
Using a rodent model, the researchers showed that doxorubicin increases CDK2 activity in cardiac muscle cells, resulting in cell death. What’s more, they demonstrated that suppressing CDK2 levels alleviated damage to cardiac muscle cells following treatment with doxorubicin.
Published in the Journal of Biological Chemistry, their finding could be used as the basis for future development of treatment strategies and drugs to reduce heart disease risk in cancer survivors, especially those treated in childhood.
Heart disease after cancer treatment
Recent improvements in the diagnosis and treatment of cancer have increased the survival odds of cancer patients. In the U.S., an estimated 16 million people — or 5 percent of the population — are cancer survivors. After cancer recurrence, heart disease is the number one cause of death in this group. Heart toxicity associated with the use of doxorubicin and related chemotherapy drugs is thought to be responsible for cancer survivors’ increased risk of developing heart disease.
Read more at Washington State University
Image: Assistant professor Zhaokang Cheng and postdoctoral fellow and co-author Peng Xia examine bacterial cultures used to grow genes of interest to their research, such as the CDK2 gene. The genes are then isolated and introduced into cardiac muscle cells to study their function. (Credit: Photo by Cori Kogan, Washington State University Health Sciences Spokane)
