Researchers have developed a new molecule that can stop the progression of heart failure

Heart failure occurs when the heart is unable to pump enough blood and oxygen to support the body's other organs due to its systolic and (or) diastolic functions are impaired. Heart failure is a serious disease. But it doesn't mean the heart has stopped. Heart failure is a chronic disease that worsens over time. Statistics show that about half of the patients die within 5 years.

Cardiovascular disease kills 17.9 million people a year, or 31 percent of global deaths, according to the world health organization. Subsequent acute myocardial infarction in heart failure is the leading cause of morbidity and mortality worldwide.

A group of researchers in Brazil and the United States has developed a molecule that blocks the progression of heart failure and improves the heart's ability to pump blood. Their findings have been published in Nature Communications.

The molecule is called SAMβA, and its name represents "selective antagonist of mitofusin 1-β2PKC association", referring to its ability to inhibit the interaction between the common protein kinase C beta 2 (β2PKC) and MFN1 (mitochondrial protein 1) in heart cells. MFN1 is a key element in mitochondria, the organelles that produce energy for cells.

In this interaction, β2PKC inhibits MFN1 and prevents mitochondria from producing energy, thereby reducing the pumping action of the heart. Its key role in the progression of heart failure was previously unknown.

Previous studies by one of the groups have shown that inhibiting the overproduction of β2PKC in heart failure cells improves cardiac function in these patients. However, the intervention prevented the protein from working in other ways that would benefit the heart.

The team first conducted different experiments to test the interaction between β2PKC and Mfn1. They found that six molecules inhibited the interaction, but only SAMβA selectively repressed the interaction of β2PKC with MFN1 in the mitochondria and did not affect other functions of the protein.

Next, they tested SAMβA in human heart cells. The molecule not only stopped the progression of the disease that drugs currently in use have already achieved, but it also improved the capacity of cells to contract - an essential part of the heart's job of pumping blood throughout the body.

In addition, SAMβA also reduced the amount of hydrogen peroxide in the mitochondria of heart cells. The presence of this peroxide indicates oxidative stress, which is a trigger for myocardial cell degeneration.

Following, the researchers implanted osmotic pumps under the skin of rats with heart failure to release small amounts of SAMβA or harmless substances for six weeks. Compared to the control group, rats treated with SAMβA ceased to exhibit heart failure and their heart function improved.

The next step is to make SAMβA available to other research groups to test for other diseases in different experimental models. It also needs to test how the molecules interact with drugs currently used to treat heart failure.