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New research could lead to personalized treatment for heart failure

A new study has identified a key molecule that contributes to heart failure in patients over 65.

By Amy Wallace
This is a microscopic image of the myocardium in the ventricular wall of a patient with heart failure. Red tissue corresponds to fibrosis of the heart muscle. Researchers have found a key molecule that could lead to personalized treatment of heart failure. Photo by CIMA researchers.
This is a microscopic image of the myocardium in the ventricular wall of a patient with heart failure. Red tissue corresponds to fibrosis of the heart muscle. Researchers have found a key molecule that could lead to personalized treatment of heart failure. Photo by CIMA researchers.

Jan. 24 (UPI) -- An international team of researchers has uncovered a molecule that could help lead to personalized treatment for heart failure.

The team included researchers from Indiana University, Stanford University, the Charite University Medicine Berlin in Germany and the University of Navarra in Spain.

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Heart failure is a malfunction of the heart supplying enough blood to the body for proper organ function.

"This is a great challenge for society: It is the leading reason for the hospital admission of over 65's, the cause of 3 percent of all admissions and absorbs 2.5 percent of the global healthcare budget," Dr. Javier Diez, director of the Cardiovascular Disease Program at the Center for Applied Medical Research, or CIMA, director for Research and Innovation of the Cardiology and Cardiac Surgery Department of the Clinical Universidad de Navarra and co-author of the study, said in a press release.

"In view of this challenge, on the one hand existing healthcare resources must be optimized in order to reduce the number of new cases and improve the prognosis and quality of life of HF patients, and, on the other, to research the mechanisms that produce heart failure in order to develop treatments that are more effective and safe that the ones that exist at present."

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Researchers found that an excess of a the lysyl oxidase-like 2 molecule creates fibrosis of the cardiac muscle impeding normal functioning and contributing to the development of heart failure. The research showed that by eliminating this excess, the fibrosis is repaired and heart function returns to normal preventing the onset of heart failure.

"These results suggest that the lysyl oxidase-like 2 enzyme may be a target for the treatment of this disease," Diez said.

The next step in the research is to develop testing and personalized treatment for individual patients with heart failure or to prevent heart failure.

The study was published in Nature Communications.

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