Enzymes Found to Protect Heart Cells from Chemotherapy Damage
Researchers from the University of Illinois Chicago have made a significant discovery that sheds light on how enzymes can help prevent heart damage in cancer patients undergoing chemotherapy. The study, published in Nature Communications, reveals that certain enzymes located in the mitochondria, the energy-producing powerhouses of cells, can move into the nucleus of heart cells under stress caused by certain chemotherapy drugs. This protective mechanism keeps the heart cells alive and offers new insights into potential treatments for chemotherapy-induced heart failure.
According to co-senior author Sang Ging Ong, assistant professor of pharmacology and medicine, the effectiveness of chemotherapy has led to an increasing number of cancer survivors. Unfortunately, many of these survivors develop heart failure as a result of the treatment. This has prompted the emergence of the field of cardio-oncology, which focuses on understanding how chemotherapy drugs damage heart cells. However, this research team took a different approach and sought to understand why some patients’ heart cells remain unharmed.
The initial finding was that when heart cells were subjected to chemotherapy-induced stress, the enzymes found in the mitochondria moved into the nucleus—an unusual occurrence. The researchers wanted to determine whether this movement caused the damage or protected the cells. Dr. Jalees Rehman, co-senior author and head of the UIC Department of Biochemistry and Molecular Genetics, stated that this mechanism appears to be a novel way in which heart cells defend themselves against chemotherapy-induced damage.
This discovery opens up potential clinical applications. For instance, doctors could evaluate individual patients to determine whether their heart cells, derived from personalized stem cells, possess the ability to protect themselves by moving enzymes from the mitochondria to the nucleus. This could be achieved by extracting blood samples from patients, generating stem cells from those blood cells, and then producing heart cells with the same genetic profile as the patient’s own cells.
Dr. Rehman explained that assessing the damage caused by chemotherapy and monitoring enzyme movement from the mitochondria to the nucleus in heart cells in a laboratory setting could help predict a patient’s likely response to treatment. In cases where inadequate protection is observed, it may be possible to enhance the heart cells’ defense mechanism by increasing enzyme movement and protection.
The research team is eager to conduct further investigations into whether this method can also prevent heart damage in other conditions such as high blood pressure and heart attacks. Additionally, they aim to explore the effectiveness of this protective mechanism in other types of cells like those found in blood vessels.
By uncovering this novel protective mechanism, the researchers have provided a glimmer of hope for cancer patients undergoing chemotherapy. The potential to safeguard heart cells from damage opens up new possibilities for personalized treatments and could significantly improve the quality of life for cancer survivors. However, further research is needed to fully understand the implications and clinical applications of this groundbreaking discovery.
