eMedicineLive

In an important breakthrough, scientists working at the Max Planck Institute of Heart and Lung Research have identified a protein which may play a crucial role in the way heart repairs itself after conditions causing cardiac insult. The protein, called as Oncostatin M, helps the damaged cardiac muscle cells to de-differentiate themselves, a process which helps the heart to self heal itself.

 

Cardiac muscles undergo extensive damage following a heart attack. In order to retain their functionality, the damaged muscle cells have to be replaced by new ones. In animals like salamander, the damaged cells regress to the embryonic state. The embryonic cardiac cells then produce stem cell markers and start dividing again. The new cells, produced after this process of de-differentiation, are healthy, and retain their cardiac function through remodeling of the cardiac muscles. Until now, this process of de-differentiation and then production of healthy cardiac cells was not recognized in humans.

 

However, the new study has been able to identify the protein responsible for the regeneration of cardiac muscle cells in humans. Scientists noted the presence of huge amount of oncostatin M in the heart of patients who had suffered myocardial infarction. They treated cells of cardiac muscles, which had been artificially cultivated in the laboratory, with oncostatin. They were surprised to find that most of the cells underwent de-differentiation within 6 days. Various series of stem cell markers were also seen in these de-differentiated cells. Their presence implied that the cells were ready to differentiate into healthy cardiac cells, a sign of self repairing. 

The scientists also compared the effect of oncostatin in two sets of damaged cardiac cells in rats- the first set was genetically modified in a manner that oncostatin could not produce any change in them. After treated both the sets with oncostatin, the researchers noted that most of the rats with cardiac cells amenable to treatment with oncostatin survived beyond 4 weeks of myocardial infarction, whereas, among the group where oncostatin could not produce any effect, 40% of rats died. In view of these findings, the scientists are planning to use oncostatin in the treatment of myocardial infarction.

 

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