[ad_1]
Studies on fragments of one heart replaced by another during a transplant have revealed one of the causes of the progression of heart failure and to develop a molecule to treat this disease [19659002] The work was done by researchers from the Universities of São (USP) and Stanford in the United States, and was published Jan. 18 in the journal Nature Communications
As its name indicates, the Heart failure is characterized by the low ability of the latter to pump blood to the rest of the body and can be caused by a heart attack, hypertension or organ valve problems. This is the last phase of several cardiovascular diseases, which kills the most in the world. According to the World Health Organization (WHO), an estimated 17.7 million people died worldwide because of them in 2015.
During the research, which began In 2009, scientists, led by Brazilian Julius Caesar Batista Ferreira, of the USP Institute of Biomedical Sciences (ICB), discovered a mechanism that advances heart failure. It is the interaction between two proteins, the Beta 2 kinase (Beta2PKC) and the Mitofusin 1 (Mfn1), inside the mitochondria, the organelle of the responsible cell. of energy production for the functioning of the human organism, including the heart [19659002] According to Ferreira, when the two proteins interact, Beta2PKC disables Mfn1, which interferes with the functioning of the mitochondria and l & # 39; 39, prevents the production of energy. As a result, it decreases the contraction and expansion capacity of the heart muscle cells and, consequently, the pumping of the blood.
"This interaction between the two proteins, hitherto unknown, was not as important in the progression of insufficiency.was one of the major discoveries of our work," says the researcher .
After deactivating Mfn1, Beta2PKC begins to accumulate inside the mitochondria. In previous work, the team led by Ferreira had already succeeded in inhibiting this second protein and this process of accumulation.
"The problem is that this solution also prevented Beta2PKC from exercising its own functions, beneficial for the functioning of the heart muscle," explains Ferreira
. researchers have developed the new molecule, which acts selectively, preventing only Beta2PKC from deactivating Mfn1 in mitochondria. To create it, the researchers tested recombinant proteins (produced by genetic engineering, that is, artificially from cloned genes), cells and pieces of human heart tissue with deficiency and animals.
The baptized molecule is born. of SAMbA, acronym for selective antagonist of mitofusin 1 and Beta2-PKC combination – or selective antagonist of the badociation of myocytes 1 and Beta2PKC. This name was not created by chance.
"As it was an important work done in Brazil, I thought nothing was more right than leaving a Brazilian mark in this story," Ferreira explains.
"We give a lot of value"
Ferreira explains that SAMbA was synthesized in the laboratory from peptides (protein parts), in the laboratory and in the laboratory, in order to maintain the right heart rate. that act on the heart cells and are designed to block the interaction between Beta2PKC and Mfn1. First of all, in vitro tests were performed. In total, six molecules were created and tested. All inhibited the interaction between the two proteins, but only SAMbA did so selectively, preventing Beta2PKC from disabling Mfn1.
The next step was to test the new molecule, still in vitro, directly on human heart cells.
"The results showed that he was able to prevent the progression of heart failure, as well as to improve the ability of cardiac cells to contract and expand, which is necessary to pump blood to the rest of the body, "he says. Ferreira
Finally, SAMbA was tested in rats, in which an infarction was induced, which resulted in heart failure in rodents. They were divided into two groups and for six weeks, one received a treatment with the new molecule and the other, which served as a control, a placebo (no effect substance).
Among those who were actually treated, the disease was
"Current drugs prevent the progression of heart failure, but never make it regress," reports Ferreira
. "Our work shows that by preventing SAMbA interactions not only reduces progression, but also makes the disease less serious between Beta2PKC and Mfn1 proteins."
Ferreira attributes the good results of the new molecule to a unique feature of it. "Current drugs act on the outside of the diseased cell, specifically on its membrane," he says.
"They do not act in the cell itself.
Despite the good results, it will take some time for the molecule developed by the Ferreira group to give birth to a new drug against cancer. heart failure
] "What we have for the moment is a prototype," he says.
"We must now enter the development phase. Transform SAMbA into drugs is another eight years of research, possibly in partnership with the pharmaceutical industry, you must also check your interaction with other drugs that the patient takes, because it must have an additional effect on them. can not take the medications they take to test it. "
Of all In all cases, the SAMbA patent has already been applied to the United States.
" We are already discussing with some pharmaceutical companies that have shown interest in advancing studies on the molecule that we have created and to transform it. in a new drug, "says Ferreira
" But as it is a new treatment for humans, it takes time. "
BBC Brasil – All rights reserved – Reproduction is prohibited without the written permission of the BBC
Source link
