- A study from the Department of Clinical and Molecular Cardiovascular Research, Keio University School of Medicine, Shinjuku-ku Tokyo, Japan; Department of Cardiology, Keio University School of Medicine, Shinjuku-ku Tokyo, Japan; and JST CREST, Shinjuku-ku Tokyo, Japan has reported that “MiR-133 promotes cardiac reprogramming by directly repressing Snai1 and silencing …”
- This study was published in the 11 June 2014 EMBO Journal by Prof. Ieda M, Muraoka N and others from the Department of Clinical and Molecular Cardiovascular Research, Keio University School of Medicine, Shinjuku-ku Tokyo, Japan Department of Cardiology, Keio University School of Medicine, Shinjuku-ku Tokyo, Japan.
- On the foundation of this interesting finding, Dr L Boominathan, Director-cum-chief Scientist of GBMD, reports here that:Therapeutic insights into making the highly efficient cardiomyocyte-like cells from differentiated cells: Pro-inflammatory protein TNFα inhibits cardiac reprogramming by increasing Snai expression. This study suggests that TNF-α, by increasing the expression of its target gene, it could decrease the number of beating cardiomyocyte-like cells (iCMs). Taken together, this study suggests that (1) pharmacological formulations containing “TNF-α or its inhibitors“ can be used to increase the number of beating cardiomyocyte-like cells (iCMs); and (2) TNF-1α inhibitors can be used to promote cardiac repair.
Idea Proposed/Formulated by: Dr L Boominathan Ph.D.
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To cite: Boominathan,Therapeutic insights into making the highly efficient cardiomyocyte-like cells from differentiated cells: TNFα inhibits cardiac reprogramming by increasing Snai expression, 09/July/2014, 5.55 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
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