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Stem cells genetically engineered to speed up myocardial repair and treat heart disease
Stem cells genetically engineered to speed up myocardial repair. As we all know, cardiovascular disease is the number one cause of death in the world.
Heart disease is one of the important factors. An early challenge in the treatment of heart disease has always been the death of part of the heart muscle after a heart attack. The heart cannot regenerate muscle tissue. The dead muscle tissue can also cause damage to the surrounding muscles, which can lead to fatal The heart is dilated.
For a long time, cardiologists have tried to repair the heart in two ways. One is to inject heart cells to replace the damaged myocardium, and the other is to activate the division of myocardial cells near the damaged area to compensate for the damaged myocardium.
Recently, the team of Professor Jianyi Zhang from the University of Alabama at Birmingham published a research paper titled “Cyclin D2 Overexpression Enhances the Efficacy of Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes for Myocardial Repair in a Swine Model of Myocardial Infarction” in the journal Circulation. .
The research team injected cardiomyocytes differentiated from artificial induced pluripotent stem cells (iPSC) overexpressing the human cyclin D2 gene into a pig model of heart disease, and found that it can effectively promote cardiomyocyte proliferation and accelerate heart repair. Cardiomyocytes promote the repair of cardiomyocytes around damaged tissues through miRNA carried in exosomes. It provides a new potential strategy for the repair and treatment of heart diseases such as myocardial infarction.
In this study, the research team used a pig model of heart disease for experiments. Compared with the mouse study, the pig’s heart is more similar in size and physiology to the human heart, so it is more clinically relevant to human diseases.
After an experimental heart attack in a pig model, the research team injected about 30 million bioengineered human cardiomyocytes into the heart tissue around the site of myocardial infarction. These cells were further differentiated by artificially induced pluripotent stem cells (hiPSC). Come. These cells also overexpress the human cyclin D2 gene (Cyclin D2), which is a member of the protein family involved in cell division.
Compared with control human cardiomyocytes, cardiomyocytes overexpressing human cyclin D2 gene (Cyclin D2) showed a stronger ability to repair the heart. They proliferate rapidly after injection, and by four weeks, the pathogenicity of the heart becomes smaller, the dead muscle tissue is reduced, and the heart function is improved.
Interestingly, cardiomyocytes overexpressing the human cyclin D2 gene (Cyclin D2) not only stimulate their own proliferation, but also stimulate the proliferation of other cardiomyocytes around the porcine myocardial infarction site, and show angiogenesis and new blood vessel development.
Professor Zhang Jianyi, the corresponding author of the study, said that these results may be a potential therapeutic strategy for repairing the heart after myocardial infarction by transplanting cardiomyocytes that overexpress the human cyclin D2 gene.
Professor Zhang Jianyi
The research team further discovered that cardiomyocytes overexpressing the human cyclin D2 gene (Cyclin D2) promoted the proliferation of nearby cardiomyocytes through secreted exosomes. The research team purified exosomes from cultured cardiomyocytes overexpressing the human cyclin D2 gene (Cyclin D2) and found that the exosomes can indeed promote the proliferation of cultured cardiomyocytes. And further revealed that exosomes play a role by carrying miRNA.
Finally, the corresponding author Professor Zhang Jianyi said that the combination of exosomal delivery of proliferative miRNA and cardiomyocyte transplantation overexpressing human cyclin D2 may become a new promising treatment for promoting cardiomyocyte proliferation and repairing heart disease. Strategy.
All in all, these research data indicate that the use of cardiomyocytes with strong proliferation capacity may be an effective treatment strategy for myocardial repair and prevention of congestive heart failure in patients with acute myocardial infarction.
(source:internet, reference only)