In the journal Circulation, authors reveal an exciting new avenue of research into repairing damaged hearts. Latest research highlights the critical role of cardiomyocytes and mitochondria in heart regeneration. Research shows that regulating mitochondrial activity can enhance heart repair after damage and provide new ideas for the treatment of heart disease.

These tiny "natural batteries" allow this vital organ to beat 100,000 times a day and pump 2,000 gallons of blood through the body.

But devastating damage occurs when these batteries - heart muscle cells called cardiomyocytes - short-circuit and die. The damage to the heart muscle is usually permanent, preventing the heart from pumping blood properly.

That's the subject of a new study by a team including two doctors from the University of South Florida (USF) Health, who report their findings in Circulation, the American Heart Association's flagship journal.

"An injury like a heart attack results in a massive loss of heart muscle cells that cannot regenerate," said Dr. Da-Zhi Wang, director of the Center for Regenerative Medicine at the University of South Florida's Healthy Heart Institute and Morsani College of Medicine. "So the question is how to get the heart to repair itself."

Progress in cardiac regeneration research

Dr. Wang's research laboratory recently relocated to USF from Harvard Medical School, where he was a professor at Boston Children's Hospital. Dr. Wang is currently a professor of Internal Medicine and Molecular Pharmacology and Physiology at Morsani School of Medicine and is the senior author of the study "Reduced Mitochondrial Protein Translation Promotes Cardiomyocyte Proliferation and Heart Regeneration." The paper discusses how the activity of mitochondria, which are found within heart muscle cells, is critical to repairing damaged hearts and even preventing future heart attacks or coronary heart disease.

Dr. John Mably, another author of the study, said: "The key element of this study is the link to heart regeneration. If you want your heart to continue to work well into your 90s, this will be of interest to you or anyone who has had heart disease or a heart attack."

Dr. Mably is an associate professor of internal medicine at the Morsani School of Medicine and a member of the Center for Regenerative Medicine and the USFHealth Heart Institute. The USFHealth team received funding from the USFHealth Heart Institute at the Morsani School of Medicine and the National Institutes of Health. Dr. Jinghai Chen of Zhejiang University School of Medicine (who trained with Dr. Wang) and members of his laboratory are also authors of the paper.

Understanding the role of mitochondria in heart function

Cardiomyocytes are an integral part of heart tissue and are critical to the normal function of the heart. Because the heart is constantly contracting, it requires large amounts of energy, which is produced by mitochondria, tiny subcellular structures often referred to as the powerhouses of the cell. Because mitochondrial protein synthesis is critical to its structure as well as normal heart function, the authors' research focused on how changes in mitochondrial protein balance affect heart health.

Dr. Mably added: "The heart muscle contracts from early development to death, so it requires a lot of energy to run. That's what the mitochondria provide; it's like the gasoline a car needs to run."

The importance of mitochondria in normal heart function is well recognized, and recent studies have shown that changes in mitochondrial metabolism are associated with some forms of heart disease. This work evolved from a previous study by the research team. Their research shows that the absence of a protein called MRPS5 in the developing heart leads to heart defects and embryonic death; the absence of this gene at all stages after birth leads to heart enlargement and eventual failure. The cause of these heart malformations was shown to stem from an imbalance in communication between mitochondria and the nucleus.

In the new study, the authors examined the effects of reduction (rather than complete loss) of MRPS5 on cardiomyocyte proliferation. Severe damage to the heart, usually from a serious heart attack, can lead to heart failure because the heart can no longer contract properly. This is because damaged tissue in the adult myocardium (the muscle layer of the heart) cannot repair itself after an injury. These scientists have found that slightly reducing the activity of mitochondria in the adult heart can promote heart regeneration after injury, which could open up a new way to treat heart disease and other heart diseases.

"We hope to work with the pharmaceutical industry to learn how to better protect or repair damaged hearts. Currently, clinicians can only do so much about heart attacks. This approach could help the heart return to normal," said Dr. Wang.

"Like the Energizer Bunny, this could lead to a new way to treat heart disease, allowing aging hearts to "keep growing, keep growing..."

Compiled source: ScitechDaily