Molecular therapy for Myocardial Infarction: Exenatide (brand name: Byetta, & Bydureon), a hypoglycemic agent that functions as a glucagon-like peptide-1 agonist (GLP-1 agonist), inhibits DNA damage responses, increases telomerase expression, inhibits telomere shortening, and promotes cardiomyocyte survival after myocardial infarction via up-regulation of PNUTS, 21/January/2017, 2.10 pm

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What they say

A recent study from the Institute for Cardiovascular Regeneration, Centre of Molecular Medicine, Frankfurt, Germany shows that “MicroRNA-34a regulates cardiac ageing and function.” This study was published in the 7 March  2013 issue of Nature  by Prof Dimmler, Boon, and others.


What we say

On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: Molecular therapy for Myocardial Infarction: Exenatide (brand name: Byetta& Bydureon), a hypoglycemic agent that functions as a glucagon-like peptide-1 agonist (GLP-1 agonist), inhibits DNA damage responses, increases telomerase expression, inhibits telomere shortening, and promotes cardiomyocyte survival after myocardial infarction via up-regulation of PNUTS


From Significance of the study to Public Health relevance:

Given that: (1)  cardiovascular disease is the leading cause of death worldwide; (2) the raise of death rate, due to cardiovascular disease, has increased from  123 lakhs in 1990 to 173 lakhs in 2013; (3) 85% of people over 80 years are susceptible to cardiovascular diseases;(4) in India, in 2004, 14.6 lakhs deaths (14% of total deaths) were due to ischemic heart disease; (3) the death due to cardiovascular disease is higher in low-to-middle income countries compared to developed countries; (4) the global economic cost spent in the treatment of cardiovascular disease in 2011 was little more than 10 billion US dollars; (5) an alarming number of people, such as 230 lakhs people, will die from cardiovascular diseases each year by 2030, there is an urgent need to find: (i) a way to induce regeneration of cardiomyocytes that were lost in Myocardial patients; (ii) a cheaper alternative to the existing expensive drugs; and (iv) a side-effect-free Natural product-based drug.


From Research Findings to Therapeutic Opportunity

Exenatide, by decreasing the expression of its target genes, it may increase the expression of PNUTS and the cellular immortality gene TelomeraseThereby, it may: (1) inhibit DNA damage responses, (2) increase Telomerase expression; (3) inhibit telomere shortening; (4) augment insulin sensitivity; and (5) promote cardiomyocyte survival/regeneration (figure 1).

Exenatide suppresses PNUTS expression

Figure 1. The anti-hypoglycemic medication Exenatide functions as a cardioprotective agent. Mechanistic insights into how Exenatide induces the expression PNUTS and Telomerase to promote Cardiac regeneration and survival and insulin sensitivity

Thus, by treating myocardial patients with Exenatide or its analogs either alone or in combination with other drugs (figure 1), one may prevent ageing-associated (or, stress-associated) decline in cardiac function. 

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Together, this study suggests that pharmacological formulations encompassing Exenatide   or its analogs or Exenatide  plus any of the known drugs that improve myocardial function”  may be used to improve cardiac function after myocardial infarction.  


Details of the research findings

Idea Proposed/Formulated (with experimental evidence) by:

Dr L Boominathan Ph.D.

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

Undisclosed mechanistic information: How does Exenatide  increase the expression of PNUTS and Telomerase?

Amount: $100#

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# Research cooperation


References:

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

CitationBoominathan, L.,  Molecular therapy for Myocardial Infarction: Exenatide (brand name: Byetta& Bydureon), a hypoglycemic agent that functions as a glucagon-like peptide-1 agonist (GLP-1 agonist), inhibits DNA damage responses, increases telomerase expression, inhibits telomere shortening, and promotes cardiomyocyte survival after myocardial infarction via up-regulation of PNUTS, 21/January/2017, 2.10 pm,  Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

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