Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports here that: Molecular therapy for Myocardial dysfunction: MiR-26 increases CDK inhibitor p27 expression, inhibits mTOR pathway, promotes autophagy in myocardial cells and prevents myocardial dysfunction via down-regulation of its target gene
Given that: (1) cardiovascular disease is the leading cause of death worldwide; (2) in India, in 2004, 14.6 lakhs deaths (14% of total deaths) were due to ischemic heart disease; and (3) the global economic cost spent in the treatment of cardiovascular disease in 2011 was little more than 10 billion US dollars, there is an urgent need to find: (i) a way to induce regeneration of adult cardiomyocytes that were lost in Myocardial patients; (ii) a cheaper alternative to the existing expensive drugs; and (iii) a side-effect-free drug.
MiR-26, by decreasing the expression of its target gene, it may: (1) increase the expression of marker of autophagy LC3-II, 2) inhibit selective autophagy receptor p62/sequestosome 1 (SQSTM1) expression, 3) inhibit the expression of negative regulator of autophagy, mTOR, 4) promote autophagy, 5) increase CDK inhibitor p27 expression, 6) decrease left ventricular end-diastolic internal diameter and heart size, and (5) inhibit cardiomyocyte dysfunction. Together, this study suggests that pharmacological formulations encompassing “MiR-26 activators” may be used to improve cardiac function.
Idea Proposed/Formulated by: Dr L Boominathan Ph.D.
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Citation: Boominathan, Molecular therapy for Myocardial dysfunction: MiR-26 increases CDK inhibitor p27 expression, inhibits mTOR pathway, promotes autophagy in myocardial cells and prevents myocardial dysfunction via down-regulation of its target gene, 26/October/2016, 8.50 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
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