In an article published in the journal Science Immunology, Universidade Federal de Sao Paulo (UFS) researchers (who are leading research on human blood vessel development) propose a strategy to replace, or reactivate, some of the symptoms of myocardial infarction (MI) by boosting a protein called TRAF8 that actually suppresses its central counterpart in the blood vessel cells. This prevents excessive vasoconstriction and protection against ventricular failure. This application for the treatment of MI is intended to begin in the next five years.
The main challenges for treating MI patients include the fact that a large number of patients do not respond adequately to anti-angiogenic drugs; researchers cannot reduce the dosage of the anti-angiotensin-converting enzyme 2, or ACE2, inhibitor.
TRAF8 makes plasma cells into cardiomyocytes, the cells found in the heart; this makes them important for the processes of heart development, including the initial beating of the heart. However, in this case an increased 7-day accumulation of missing information about the total number of active cells in the vascular system causes a severe cardiac failure. In addition, TRAF8 inhibitors are not very effective in the preclinical or in animal models.
VivaViva is one of the first companies that produces the first human monoclonal antibodies against TRAF8. Other companies such as Oscar de La Hoya, VivaVita, and Vella Therapeutics are working towards the development of treatments that will target either the TRAF8 enzyme or also’ the part of the protein that suppresses it.
There is no cure for MI but the prevention of associated obstruction by an extensive blockade of vascular function can reduce the severity. As a matter of fact, the isolated TRAF8 protein could potentially be approved for the treatment of patients with congestive heart failure.
