According to a recent research study published in the journal Circulation Research, the aging of the heart is linked to the emergence of heart failure and associated cardiac hypertrophy. The study found that a dysfunctional change in organ metabolism leaves the heart without the energy needed to pump blood efficiently. Researchers have identified a switch that governs this change in metabolism and have shown that inhibiting its action can improve heart function, at least in laboratory studies.
The research was coordinated by Gianluigi Condorelli, director of the Cardio Center at Humanitas and head of the Laboratory of Immunology and Inflammation in Cardiovascular Diseases. He collaborated with Roberto Papait, an associate professor at the University of Insubria.
Heart failure is a widespread and disabling condition, with 600,000 people living with it in Italy alone. It is the main cause of disability and death among elderly individuals in industrialized countries. While there are currently therapies available to slow down the progression of the disease, the search for new and more effective therapeutic solutions remains a major challenge in cardiology.
The studies conducted over the past twenty years have revealed that heart failure is fundamentally an energy problem. The heart, being one of the most energy-intensive organs in the body, requires a significant amount of energy to pump blood and sustain its function. Several drugs used in heart failure treatment work by allowing the heart to save energy, but the reduction in available energy resources and why it occurs more frequently with aging has remained unclear.
The research study has revealed that a gene enhancer called p300 plays a role in regulating the heart’s energy balance. During aging, the activity of p300 intensifies and alters the metabolism of heart cells, leading to a reduced oxygen supply and a shift in energy needs to the consumption of sugars, which are a less efficient energy source. This leaves the heart without the necessary energy and contributes to the onset of heart failure.
In laboratory models of the disease, researchers have successfully turned off the action of p300 using an inhibitor, resulting in a partial recovery of cardiac function. Although this study is limited to laboratory models, the results provide new avenues for research into the treatment of heart failure.
The discovery of this link between aging and heart failure provides a piece of the complex puzzle and opens up potential for the development of new therapies to reduce the risk of heart failure in old age. Further research and clinical trials will be needed to explore the full potential of targeting p300 as a therapeutic approach for heart failure.
Overall, this research study sheds light on the underlying mechanisms of heart failure and presents promising possibilities for improving heart function in the aging population.