New Protein Named Oncostatin M, Demonstrates Its Beneficial Effects After Miocardial Infarction

New Protein Named Oncostatin M, Demonstrates Its Beneficial Effects After Miocardial Infarction

Even if even if there are many methods of reperfusion after a heart attack, cardiac muscle dysfunction occurs in most cases, as myocytes do not regenerate. In vertebrates, for example salamanders, a mechanism of regeneration of myocardium based on a process called dedifferentiation was discovered, allowing healthy cells to regress to embryonic stage, divide and the differentiate to myocytes, thus restoring myocardial function. In humans, cardiac stem cells have been identified, but their exact role in restoring myocardium functionality after a heart attack is not yet established.

The research group from the Max Planck Institute, led by Dr. T. Braun, discovered that the molecule which appears to be responsible for  cardiomyocyte dedifferentiation process is a protein called oncostatin M. The study started from the fact that human myocardial tissue contains higher concentrations of oncostatin M after a heart attack. The researchers designed a study to see if oncostatin M has the same benefits in mammals. Two groups of mice, a normal one and a genetically modified mice group so that oncostatin M could not have any effect.  The scientists then induced a heart attack to all mice. In the normal mice group, the oncostatin M demonstrated its effects.

Myocardial infarction 4

Dr. Braun concluded that “We believe that oncostatin M has considerable potential for efficiently healing damaged heart muscle tissue. What we now need is to be able to pinpoint the precise window of application to prevent any possible negative effects.”

A potential disadvantage is that in coronary chronic diseases, oncostatin M can potentially exacerbate the prejudice caused by myocardial infarction.

Although potential harmful effects of oncostatin M have been observed,  this new discovery could mean another step forward towards  development of new therapies for myocardial infarction and restoration of cardiac function after the occurrence of an injury.

Myocardial infarction (heart attack) is the result of coronary artery obstruction due to atherosclerosis, thrombus or vasospasm, which translates to decreased blood flow to the myocardium, thus reducing the intake of oxygen and nutrients, leading to myocardial cell death.  Myocardial infarction is a common cause of mortality in older age groups. So far the area affected by infarction can be reduced by reperfusion of myocardial tissue, in addition to early intervention with coronary vasodilators, antiplatelet agents, oxygen and other medication but there is still no satisfactory therapy for large infarctions.