Stem Cell Combination Therapy with Enzyme Inhibitors Leading towards Declined Rate of Heart Attacks

Release Date: 19-Nov-2020

For the treatment of damaged heart tissues, blocking an enzyme related with inflammation is believed to be useful as it will lead to the stem cells to repair it. The respective enzyme that is believed to be effective in case of treating the damaged heart tissues is soluble epoxide hydrolase. Since the information gathered for the enzyme, it has become one of the most focused clinical research areas for the researchers who are aligned towards treating heart disease. As per the researchers, it is estimated that the evaluation of the enzymes will lead to the development of novel class of compounds that will reduce the mortality rate due to heart failure.

The researchers involved in this believe that they have found a novel way to provide stem cells a chance to heal the heart tissues that have been damaged due to any reason. The similar hypothesis has been tested in mice model using cardiac muscle cells known as cardiomyocytes which were initially derived from human induced stem cells. In the respective study, dozens of enzyme inhibitors were also tested. It was concluded by the researchers that the mice group that received combination of the inhibitor and hiPSCs delivered beneficial outcomes with respect to the survival of the stem cells that have been transplanted and increased engraftment. Heart muscle thickening as well as improved cardiac function was also observed in the similar mice group.

Therefore, it was stated that the combination of hiPSC cardiomyocytes with with sEH inhibitors led to better survival rate in the muscle damaged by a heart attack. The overall outcomes received from the above-mentioned clinical trial depicts the future therapeutic treatment it carriers, therefore, the researchers involved in this will take the respective clinical research study to next step i.e. larger research animal model for providing better insights about the benefits of the combination therapy.