- A research group belonging to the Biomedicine Institute of Seville (IBiS) has described a mechanism activated after a myocardial infarction, involving the proteins Orai1, AC8, and CREB.
- These proteins are involved in the increase of calcium in the heart, which damages cardiac function and can lead to heart failure, with fatal consequences.
- Inhibiting Orai1 could be a new therapeutic strategy to prevent the progression of the disease after a heart attack, helping to reduce further damage.
Seville, March 21, 2024
Myocardial infarction is one of the leading causes of death worldwide. Nearly half of the patients with heart failure die within 5 years following the diagnosis, according to the WHO. In search of new approaches to reduce these figures, a multidisciplinary team, led by the Cardiovascular Pathophysiology Group of the Biomedicine Institute of Seville (IBiS), has recently described a possible therapeutic pathway. This involves an essential protein for the regulation of the calcium ion within cells, Orai1, which shows increased expression after a myocardial infarction.
This manifestation seems to be directly related to the possibility of suffering more severe, even lethal, consequences afterward. With the aim at a new therapeutic target, this research believes that new treatments could be prescribed with hopeful results for people affected by a myocardial infarction.
More heart failure after a heart attack
Following an episode of a heart attack, there is a high probability of developing heart failure. "When a patient survives a myocardial infarction, a few months later they develop an adaptation mechanism called remodeling," explains Tarik Smani, head of the Cardiovascular Pathophysiology Group at IBiS. "This is characterized by hypertrophy and the appearance of fibrosis necessary to repair the infarcted area." In other words, the damaged tissue is repaired by another type of tissue, akin to scar tissue, points out Débora Falcón, a researcher in the team.
According to the research team, the problem arises when this, over time, starts to affect other parts of the heart: "When these mechanisms become chronic, the adaptation turns pathological, increasing hypertrophy and fibrosis throughout the heart, which significantly affects cardiac function." It is in all this complex relationship where the protein Orai1 takes center stage.