Through improved therapy and screening available today, patients are surviving longer after cancer diagnosis. However, some cancer treatments such as doxorubicin, a bacterial antibiotic, also cause damage to the heart causing it to fail. Activating sirtuins can prevent heart failure in cancer patients
Failing hearts are like an engine running out of fuel because the heart is unable to pump sufficient blood to meet the requirements of the body. Two factors contribute to the development of heart failure. One is the inability of the heart to produce enough energy to pump blood to the rest of the body. A second is high levels of reactive oxygen species (ROS), which are by-products of oxygen that damage the heart tissue, interfering with its ability to pump blood.
Mitochondria are cellular organelles responsible for energy production as well as the major site of ROS production. Mitochondrial dysfunction is associated with heart failure though it is unknown whether mitochondrial dysfunction represents a primary cause of heart failure.
In their review article published in the journal of Biological Chemistry, the researchers studied the literature on sirtuins – proteins that regulate cardiac mitochondrial functions. The authors also evaluated the potential that sirtuin activation could rescue mitochondrial dysfunction caused by cancer treatments, and whether sirtuin activation increased the supply of fuel for the engine of the heart prevented damage by ROS. Thus, activation of sirtuins could ultimately halt the progression of heart failure by allowing it to pump blood better.
This review of the literature suggests that activation of sirtuins to prevent heart failure appears to be a highly desirable strategy. More experiments are needed to determine whether it could be successful in improving mitochondrial function, reducing ROS production and alleviating heart failure caused by the use of chemotherapeutic medications.
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