A group of scientists from Brazil and the US have created a molecule SAMβA, which stops the development of heart failure and improves the ability of the organ to pump blood. Treatment of rats with a new drug for six weeks not only stopped the disease, but also improved the condition of the body by strengthening the muscles of the heart. About it reported in a press release on MedicalXpress.
SAMβA inhibits the interaction between the molecule β2PKC — kinase-C-beta-2 — mitofusin 1 (Mfn1), a key element of the mitochondria. β2PKC Mfn1 inhibited, not allowing the mitochondria to produce energy and thus degrades the function of the heart. It is known that excess of protein kinase-C-beta-2 is associated with heart failure, and its deactivation improves the condition of patients. However, the lack of β2PKC can lead to other undesirable effects.
The new molecule has a selective effect, ie it prevents mitochondrial dysfunction, but safe for other important processes. For and search test experiments were carried out with recombinant proteins, cell cultures, animals and cardiac tissues obtained from patients. Initially it was found six molecules with similar properties, but only SAMβA did not enter into unwanted interaction.
SAMβA also reduces the concentration of hydrogen peroxide in the cells, the presence of which is associated with oxidative stress and damage to cellular components such as proteins, DNA and lipids. In rats, which was caused by myocardial infarction, the molecule stopped the development of heart failure and improved health compared with the control group, in which sick animals received a placebo.