Molecular therapy for Myocardial dysfunction: Metformin, one of the widely used drugs in the treatment of TIIDM, increases CDK inhibitor p27 expression, inhibits mTOR pathway, promotes autophagy in myocardial cells and prevents myocardial dysfunction via down-regulation of its target gene, 21/October/2016, 6.15 am

Molecular therapy for Myocardial dysfunction: Metformin, one of the widely used drugs in the treatment of TIIDM, increases CDK inhibitor p27 expression, inhibits mTOR pathway, promotes autophagy in myocardial cells and prevents myocardial dysfunction via down-regulation of its target gene, 21/October/2016, 6.15 am

Molecular therapy for Myocardial dysfunction: Metformin, one of the widely used drugs in the treatment of TIIDM, increases CDK inhibitor p27 expression, inhibits mTOR pathway, promotes autophagy in myocardial cells and prevents myocardial dysfunction via down-regulation of its target gene, 21/October/2016, 6.15 am 150 150 Dr Boomi's Genom-2-Discovery Center

Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports here that: Molecular therapy for Myocardial dysfunction: Metformin, one of the widely used drugs in the treatment of TIIDM, increases CDK inhibitor p27 expression, inhibits mTOR pathway, promotes autophagy in myocardial cells and prevents myocardial dysfunction via down-regulation of its target gene


Significance:

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.

Research Findings: 

This study suggests that a widely known anti-hyperglycemic drug functions as a myocardial protective agent.  Metformin, 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 “Metformin or its analogs” may be used to improve cardiac function.

Idea Proposed/Formulated by: Dr L Boominathan Ph.D.

Web: http://genomediscovery.org or http://newbioideas.com

Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/

Citation: Boominathan, Molecular therapy for Myocardial dysfunction: Metformin, one of the widely used drugs in the treatment of TIIDM, increases CDK inhibitor p27 expression, inhibits mTOR pathway, promotes autophagy in myocardial cells and prevents myocardial dysfunction via down-regulation of its target gene, 21/October/2016, 6.15 am,  Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

Courtesy: When you cite drop us a line at info@genomediscovery.org

# Research cooperation

Amount: $100#

Undisclosed information: How Metformin promotes autophagy in cardiomyocytes and prevents heart failure.

satisfaction-guaranted-if-not-refunded

Results guaranteed if not refunded

Share
Natural product therapy for tuberculosis: Avacado (Persea Americana) fruit extract increases the expression of MKP-1, inhibits TLR2 signalling, secretion of Chemokine CXCL5, and recruitment of polymorphonuclear leukocytes (PMNs), decreases destructive pulmonary inflammation, promotes M. tuberculosis clearance and inhibits pulmonary tuberculosis via up-regulation of its target gene, 20/October/2016, 10.51 pm
Natural product anti-inflammatory therapy for upper respiratory tract inflammatory diseases: Hyperoside, found in Drosera Rotundifolia and Prunella vulgaris (Common self-heal), increases the expression of negative regulator of inflammation MyD88(s), inhibits pro-inflammatory mediators in lungs, and alleviates the common respiratory pathogen nontypeable Haemophilus influenzae (NTHi)-exacerbated asthma & chronic obstructive pulmonary disease via up-regulation of its target gene, 21/October/2015, 7.55 am
Start Typing