Molecular therapy for Myocardial Infarction: PF-4708671, an inhibitor of p70 ribosomal S6 kinase 1, inhibits DNA damage responses, increases telomerase expression, inhibits telomere shortening, and promotes cardiomyocyte survival after myocardial infarction via up-regulation of PNUTS, 26/December/2016, 9.33 am

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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: PF-4708671, an inhibitor of p70 ribosomal S6 kinase 1inhibits 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

pf-4708671-induces-the-expresion-of-pnuts-to-prevent-myocardial-infarction

Figure 1. Mechanistic insights into how PF-4708671 induces the expression PNUTS and Telomerase to promote Cardiac regeneration and survival and longevity

This study provides mechanistic insights into how PF-4708671 may promote cardiac survival and regeneration.

PF-4708671, by regulating the expression of its target genes, it may increase the expression of PNUTS and the cellular immortality gene Telomerase. Thereby, it may: (1) inhibit DNA damage responses, (2) increase Telomerase expression; (3) inhibit telomere shortening; (4) promote cardiomyocyte survival/regeneration; (5) promote resistance to bone, immune and motor function; (6) increase insulin sensitivity; and (7) promote longevity (figure 1).

Thus, by treating myocardial patients with PF-4708671  (figure 1), one may prevent ageing-associated (or, stress-associated) decline in cardiac function. 

price-100[easy_payment currency=”USD”]

Together, this study suggests that pharmacological formulations encompassing PF-4708671  or its analogues or PF-4708671 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  PF-4708671  increases 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: PF-4708671, an inhibitor of p70 ribosomal S6 kinase 1inhibits DNA damage responses, increases telomerase expression, inhibits telomere shortening, and promotes cardiomyocyte survival after myocardial infarction via up-regulation of PNUTS, 26/December/2016, 9.33 am,  Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

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