Cardiovascular disease is a leading cause of death worldwide, as well as a major component of healthcare costs.

A new study, published in Nature Communications, has shown the efficacy of a new biological drug, a monoclonal antibody, capable of blocking fibrosis and protecting the heart muscle after myocardial infarction (or heart attack, which is the stoppage or reduction of blood flow to the heart, causing it to die.) 

Antibodies (Y-shaped proteins) produced by the body’s immune system destroy invading pathogens. Monoclonal antibodies are those produced in labs, using living cells. 

The study showed that this antibody has a doubly beneficial effect: On one hand it reduces the deposition of the fibrous tissue that limits the heart’s pump function, and on the other it promotes the survival of heart muscle cells. 

The study, led by Serena Zacchigna, head of the cardiovascular biology lab of the International Centre for Genetic Engineering and Biotechnology, Trieste, Italy, and professor of molecular biology at the University of Trieste, represents a turning point in the area of innovative cardiovascular therapies. The ICGEB is a three-country, autonomous, inter-governmental organisation with labs in Italy, India and South Africa. It operates as a centre of excellence for research, training and technology transfer to industry for sustainable global development.

“In contrast to the great social and healthcare pressure exerted by these diseases, the drugs we use to treat patients with heart disease are rather dated,” explains Zacchigna. New biological therapies are transforming oncological or hereditary disease treatments, while there are very few biological drugs for the treatment of cardiovascular disorders. “The vast majority of therapies approved to date are small chemical molecules that generally have a single target — blocking the action of an enzyme or receptor, for example. By contrast, biological drugs (recombinant proteins, gene therapy products, and cell therapy) reproduce elements that normally exist in our tissues and, therefore, have the potential to interfere with complex therapy mechanisms. However, they are more difficult to prepare and use, as well as being more expensive, making them complicated to translate from experimental studies to patients.” 

This study, which is the result of a long collaboration between the Trieste institutes (ICGEB and University of Trieste) and the University of Zagreb, Croatia, reveals the fundamental role of a family of proteins, bone morphogenetic proteins (BMPs), in the evolution of cardiac fibrosis after an ischemic event. 

In the last phase of the project, a group of cardiac surgeons from Innsbruck joined the Trieste-Zagreb axis and contributed their experiences and skills to understanding the mechanisms underlying ischemic damage and the development of innovative therapies, to validate the results of this study in other contexts of ischemia and fibrosis and to pave the way for a possible clinical application. This was made possible by the INCardio project — Innovative Therapies for Cardiovascular Disorders — led by ICGEB and financed by the European Regional Development Fund and Interreg V-A Italy-Austria 2014-2020. 

“We are confident that this work will open the door to other biological drugs in the cardiovascular sector,” says Zacchigna. 

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