Abstract Heart injuries such as cardiac arrests are one of the major causes of death in the globe. Heart injuries are fatal and in most cases, patients do not survive. Fatality of this kind has made doctors look for various ways in which they can heal their patients. Scientists have come up with new ways such as regeneration of cells. Through reprogramming the cells, the new cells replace the injured cells, which later improve cardiac function of the heart. Reprogramming of cells can also help in regeneration of other body tissues.
¶ … reprogramming the injured" discusses the issue of regenerating damaged or injured heart tissues. The article seeks to show ways of improving cardiac function. The article cites the original works of L. Qian and K. Song together with their colleagues. The authors of the article state that L. Qian and his colleagues have induced scar-forming (fibroblasts) cells to change into muscle cells in live mice's damaged hearts. Scientists refer to muscle cells as cardiomyocytes. The authors, therefore, conclude that results of the experiment provide an avenue for cardiovascular investigation in translational medicine. The article talks of the discovery of MY0D1, a transcription factor that regulates expression of genes that play significant roles in the development of skeletal muscle. The article states that scientists discovered that they could reprogram somatic cells (non-germline) to pluripotent stem cells. Pluripotent cells are important because they can transform into any cell type. This happens by expressing cocktails of transcription factors such as MY0D1.
The second article "in vivo reprogramming of murine cardiac fibroblasts into induced cardiomyocytes" discusses the reprogramming of adult cells into pluripotent cells. The authors report that cardiac fibroblasts can be reprogrammed directly into adult cardiomyocyte -like cells. This occurs in addition of Mef2c, Tbx5 and Gata4. Induced cardiomyocytes become assembled sarcomeres, binucleate and have a cardiomyocyte-like expression. The authors discover that GMT delivery decreases attenuated cardiac dysfunction by three months. This occurs after coronary litigation. During the process, the infarct size also decreases. Delivery of thymosin ?4 together with GMT results in improving cardiac function and the scar area. The authors conclude that the findings demonstrate the possibility of reprogramming cardiac fibroblasts into cardiomyocyte-like cells. This occurs in their native environment for the purpose of regeneration.
Comparison
In the first article, the authors state that cardiovascular disease leads to the increase in death rates. The second article suggests the same. In the first article, the authors state that because of the heart's inability to regenerate cells, heart injuries such as heart attacks (myocardial infarction) may heal through scar formation instead of muscle regeneration. This, according to the authors, Palpant & Murry (2012), leads to the rise of heart failure. The authors of the second article Qian & Song (2012) seek the methods in which people can heal of heart attacks. They use a number of genes in their quest. The authors induce myocardial infarction in mice by occlusion of the coronary artery. The coronary artery is the blood vessel that supplies blood to heart muscles. They then use retroviruses to introduce a transcription factor gene. Through this, they manage to heal the mice of myocardial infarction. The authors, however, disagree upon the number of genes to use. Qian uses three genes, but Song introduces a fourth gene named HAND2.
Palpant & Murry (2012) in the article suggests that if the nucleation of the growth of DNA shape is fast and the subsequent nucleation of self-assembly is unusual, then complete structures will form as compared to partial ones. Another method that can ensure the formation of complete structures is the Ostwald ripening. This mechanism ensures that complete structures gain strand from the least complete structures. In the Ostwald ripening mechanism, strands fall off the less stable structure and subsequently joining the stable strands.
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