Researchers Discover Molecular Mechanism Linking Aging and Risk of Heart Failure
A group of researchers has made an important breakthrough in understanding why the risk of heart failure increases with age. Their study, published in the journal Circulation Research, reveals the molecular mechanism that links advancing age with the development of heart failure and offers hope for improving therapies.
The study, coordinated by Gianluigi Condorelli, director of the Cardio Center of Humanitas, and in collaboration with Roberto Papait, associate professor at the University of Insubria, focused on the dysfunctional change in the heart’s metabolism that occurs with aging. This change leaves the organ without the energy it needs to pump blood efficiently, leading to heart failure and associated cardiac hypertrophy.
The researchers identified a switch that governs this change in metabolism and demonstrated that inhibiting its action improved the functionality of the heart. While the study was conducted in laboratory settings, it offers new avenues for research on the treatment of heart failure.
Heart failure is a widespread and disabling disease that affects 600,000 people in Italy alone, with one in ten individuals over the age of 65 affected. It is also the leading cause of disability and death in elderly people in industrialized countries. While there are therapies available to slow down the progression of the disease, finding more effective therapeutic solutions remains a challenge in cardiology.
The root cause of heart failure is an energy problem – a decompensated heart lacks fuel. The heart is one of the most energy-intensive organs in the body, alongside the brain and muscles. To contract 60 times a minute and supply blood throughout the vascular system requires a significant amount of energy.
Many of the drugs used to treat heart failure work by allowing the heart to save energy. However, the reduction in available energy and the increased likelihood of heart failure during aging has remained a mystery. The study found that the p300 gene enhancer, which intensifies during aging, alters the metabolism of heart cells. This change shifts their energy needs to the consumption of sugars, a less efficient energy source, contributing to the onset of heart failure.
By inhibiting the action of p300 using an inhibitor, the researchers observed a partial recovery of cardiac function. While the study is limited to laboratory models of the disease, it provides important insights into the treatment of heart failure.
Professor Roberto Papait highlights the significance of this research, stating, “Although aging is the primary cause of heart failure, the explanation for this link has long eluded doctors and researchers. Today, we know one more piece of this complex puzzle: as we age, heart cells change their energy metabolism in a disadvantageous way. This is the first step to develop new therapies that reduce the risk of heart failure in old age.”
This breakthrough in understanding the molecular mechanism behind the age-related risk of heart failure brings new hope for improved therapies. With further research, it is possible that new treatments can be developed to reduce the risk of heart failure in the elderly population.