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A team of researchers from the Universities of São Paulo and Stanford in the United States has developed a molecule that can slow the progression of heart failure and improve heart function.
The result was obtained in the rat, but shows that the molecule could be studied as a future drug. There are nowadays remedies to try to delay the deficiency, a degenerative disease – that may occur after a heart attack, high blood pressure or Chagas disease – causing the heart's heartbeat to stop.
Researcher Júlio Ferreira, Institute of Biomedical Sciences, University of São Paulo led the work that led to the development of the samba molecule, able to prevent the binding of proteins contributing to heart failure
"But with what we have today with treatment, on average 50% of patients die five years after diagnosis, it would be worse without the existing remedies, but not yet ideal," says Julio Cesar Batista Ferreira , researcher at the USP Institute of Biomedical Sciences and project leader.
The new molecule performed better than that, restoring the heart's functioning in animals. The results of the study were published in this issue of Friday 18 of the journal Nature .
The search began with a plan: to search for the causes of heart suffering, the mechanism that makes it insufficient. At the worst stage of the disease, the heart pumps so little blood that the patient has to undergo a transplant.
The team led by Ferreira then studied heart samples from individuals with heart failure who needed a transplant. They then discovered that a molecule had a key role in organ dysfunction, Beta2PKC. And from that, they developed SAMbA, an acronym for the selective antagonist of the Association of Mitofusine 1 (mfn1) and Beta2PKC.
To explain the soup in the alphabet, Ferreira coined the metaphor of the boy working in a company. "The company, in our case, is the cell of the heart, where an office worker, who represents Beta2PKC, who runs through all the aisles of the company and establishes the connection between all sectors, is working well," explains the researcher.
"But we found out that the office boy had a predilection for a branch of the company, he is a friend of the finance director, mfn1, who, instead of doing his job, talks all day with the boy of Our entire industry, in the case of our cell, is made up of mitochondria, which prevents the production of energy for the cell, "continues Ferreira.
Scientists have devised a way to avoid this link between the office worker and the finance director. SAMbA prevents Beta2PKC from binding to mfn1, but continue your work on the rest of the cell. In mice used in the study, the molecule was administered daily one month after being induced by a heart attack.
"After two months, SAMBA has not only slowed the progression of the disease, but also improved cardiac function, compared to the situation of the organ before treatment," says Ferreira.
The molecule has been patented by scientists. "The next step is to allow other researchers to test on other models and find partners who will try to turn the molecule into a drug.It's a long process that can last for ten years, but it's a potential molecule. " supplements.
