An experimental study done in mice shows a potential for preventing heart failure and improving cardiac function by blocking a protein type.

Researchers at the Cincinnati Children's Heart Institute experimented on a targeted molecular therapy that blocks fibronectin protein, which overreacts at the time of a heart attack.

Fibronectin functions as a cell adhesive that binds together collagen and other proteins essential for the migration, growth, and differentiation of heart cells.

Cell adhesion comes in the form of matrices that connect tissues, especially after an injury. Unfortunately, after a cardiac arrest, the fibronectin overreacts and overproduces connective matrices. It also causes clogging that eventually damage the heart.

Good Tissue Turned Bad

Using a donated heart by deceased patients, the researchers manufactured a peptide called pUR4 to inhibit fibronectin from overproducing connective tissues.

"Our data are a strong proof of principle and the first to show that inhibiting fibronectin polymerization preserves heart function, reduces left ventricle remodeling, and limits the formation of fibrotic connective tissue," said lead author Dr. Burns Blaxall, director of translational research at the Heart Institute and the Center for Translational Fibrosis Research.

The researchers reported that inhibiting fibronectin from overproducing matrix tissues can prevent heart failure and even improve cardiac functions.

Few effective options are available to treat heart diseases, especially for people who had previous attacks or have congenital conditions. Individuals who were born with congenital heart diseases require specialized care even when they reach adulthood.

Blaxall's team has opened the study to future investigations on the application of pUR4 in human heart cells. The study, which was published in the journal Circulation, used mouse models in a simulated heart attack. The animals then developed fibrosis and eventually had heart failure.

Leading Cause of Death

About 54 percent of mortality rate or 15 million deaths in 2015 are attributed to ischemic heart disease and stroke, according to World Health Organization.

Clinicians recommend lifestyle modification as one of the strongest forms of intervention in reducing risks of heart disease. Sedentary lifestyle, smoking, obesity, and other causative events are identified as adverse factors.

In a multicenter, randomized trial funded by the National Heart, Lung, and Blood Institute, 810 adults with Level 1 hypertension were admitted to a non-pharmacologic program.

Participants were involved in DASH diet and an established intervention group. The EST group gave individual advice on physical activities, weight loss, including caloric, alcohol, and sodium intake for a period of six months.

As a result, the DASH and EST interventions have lowered the probability of a 10-year risk for coronary heart disease by 12 to 14 percent.

"Given that heart disease remains the leading cause of death in the United States, translation of these findings into clinical practice should have a substantial public health impact," the study authors wrote.

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