In a groundbreaking study published in Circulation, a team of researchers, including doctors from USF Health, sheds light on the possibility of heart regeneration by manipulating mitochondrial protein translation. This discovery opens up new avenues for treating heart disease, including heart attack.

Led by Dr. Da-Zhi Wang, Ph.D., director of the Center for Regenerative Medicine in the USF Health Heart Institute, the study focuses on cardiomyocytes - the heart muscle cells responsible for maintaining the organ's continuous pumping action. These tiny natural batteries play a crucial role in providing energy to the heart, which requires immense amounts of energy for its daily functioning.

When cardiomyocytes are damaged or die, typically as a result of a heart attack, the heart's ability to pump efficiently is compromised. Traditionally, once these cells are lost, the damage is permanent and the heart is unable to repair itself. Therefore, the central question for researchers is how to induce the heart to repair itself.

Dr. Wang's team, whose research has consistently explored the possibilities of heart repair, delved into the activities of mitochondria residing within cardiomyocyte cells. Mitochondria, often referred to as the powerhouse of the cell, are responsible for generating energy. The study identified the crucial role of altered mitochondrial protein balance in heart health, particularly in relation to repairing a damaged heart and preventing future heart attacks or coronary disease.

Dr. John Mably, an associate professor of Internal Medicine at the Morsani College of Medicine and a member of the Center for Regenerative Medicine and USF Health Heart Institute, emphasized the significance of the study. He noted that maintaining heart functionality into old age and improving outcomes for individuals with heart disease or those who have suffered a heart attack could be significantly impacted by advancements in cardiac regeneration.

The study builds upon previous research that discovered a loss of the MRPS5 protein in the developing heart resulted in cardiac defects and eventual failure. The team explored how reducing MRPS5 levels, instead of complete loss, impacts the proliferation of cardiomyocytes. Findings revealed that a slight decrease in mitochondrial activity in the adult heart could potentially facilitate heart regeneration following injury, providing a novel approach to treating heart attack and heart disease.

Dr. Wang expressed optimism regarding the future applications of their research. Through collaboration with the pharmaceutical industry, the team aims to develop strategies to protect and repair damaged hearts. While current clinical interventions for heart attack patients have limitations, this gene therapy approach shows promising potential to enable heart growth and restore normal functionality.

The implications of this study are significant, as it offers hope for those suffering from heart disease and cardiac injury. By manipulating mitochondrial protein translation, researchers may pave the way for new treatments that could lead to heart regeneration. Just like the iconic Energizer Bunny, hearts may soon be able to keep going and going, defying the limitations of age and disease.

This study was made possible thanks to the support of the USF Health Heart Institute, the Morsani College of Medicine, and grants from the National Institutes of Health. Collaboration with Dr. Jinghai Chen and his lab at the Zhejiang University School of Medicine in China also contributed to the research.

The implications of this fascinating study provide a glimmer of hope for the millions affected by heart disease worldwide. As researchers continue to unravel the intricacies of heart regeneration, the potential to revolutionize cardiology and improve patient outcomes becomes increasingly promising.