by The human heart is a remarkable organ, beating tirelessly to pump blood throughout the body. But when the heart muscle cells, known as cardiomyocytes, become damaged or die, it can lead to devastating consequences. Traditional treatments have focused on managing heart disease and preventing further damage, but a new study published in Circulation, the flagship journal of the American Heart Association, offers hope for cardiac regeneration.
The study, conducted by a team that includes researchers from USF Health, explores the potential of repairing damaged hearts by leveraging the activities of mitochondria, the energy-producing structures within cardiomyocyte cells. Led by Dr. Da-Zhi Wang, the director of the Center for Regenerative Medicine at the USF Health Heart Institute, the research team aims to understand how to stimulate the heart to repair itself and prevent future heart attacks or coronary disease.
The key finding of the study is the link to cardiac regeneration, offering potential benefits to heart patients. Dr. John Mably, an associate professor of Internal Medicine in the Morsani College of Medicine and a member of the Center for Regenerative Medicine and USF Health Heart Institute, emphasized the importance of this research for individuals with heart disease or those who have had a heart attack. The team’s findings could pave the way for maintaining heart function into old age.
Cardiomyocytes play a crucial role in the normal function of the heart by constituting the building blocks of cardiac tissue. These cells require a significant amount of energy to continuously contract and pump blood, which is supplied by mitochondria. Therefore, any disruption in mitochondrial protein synthesis can impact heart health and function. The researchers focused on understanding how alterations in the balance of mitochondrial proteins affect heart regeneration.
The study builds upon previous research conducted by the team, which identified a protein called MRPS5 as essential for proper heart development. Loss or reduced expression of this protein led to cardiac defects and embryonic death. When MRPS5 levels were altered in adult hearts, the researchers observed an enlargement of the heart and eventual failure. This disruption was attributed to an imbalance in communication between the mitochondria and the nucleus of cardiomyocytes.
In the current study, the researchers examined the effects of decreased MRPS5 expression on cardiomyocyte proliferation. They discovered that reducing mitochondrial activity in the adult heart could facilitate heart regeneration following injury. This finding offers a potential new avenue for treating heart attacks and other heart diseases.
Dr. Wang expressed optimism about the implications of their research, highlighting potential collaborations with the pharmaceutical industry to develop therapies that protect or repair damaged hearts. Currently, the options for heart attack treatment are limited, but this new approach could pave the way for heart regrowth using gene therapy.
The potential impact of this research is significant. By unlocking the ability for damaged hearts to regenerate and repair, it opens up possibilities for prolonging the health and function of the heart. Like the Energizer Bunny, this research could lead to a new way of treating heart disease, allowing older hearts to keep on going and going.
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1. Source: Coherent Market Insights, Public sources, Desk research
2. We have leveraged AI tools to mine information and compile it
Money Singh is a seasoned content writer with over four years of experience in the market research sector. Her expertise spans various industries, including food and beverages, biotechnology, chemical and materials, defense and aerospace, consumer goods, etc.
