Molecular therapy for Myocardial Infarction: AP-1 (Activator protein-1) inhibits DNA damage responses, induces telomerase expression, inhibits telomere shortening, and promotes cardiomyocyte survival after myocardial infarction, via up-regulation of PNUTS, 13/November/2018, 11.28 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 of the journal 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: AP-1 (Activator protein-1) inhibits DNA damage responses, induces telomerase expression, inhibits telomere shortening, and promotes cardiomyocyte survival after myocardial infarction, via up-regulation of PNUTS


price-300[easy_payment currency=”USD”]

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

This study provides mechanistic insights into how AP-1 (Activator protein-1) may protect against myocardial infarction.

Figure 1.  Mechanistic insights into how AP-1 (Activator protein-1) induces the expression of PNUTS and Telomerase to prevent myocardial infarction and promote Cardiac regeneration/survival

Figure 2. AP-1 (Activator protein-1) functions as a cardioprotective agent through induction of PNUTS

AP-1 (Activator protein-1), by increasing the expression of its target genes, it may increase the expression of PNUTS (fig.1). Thereby, it may: (1) inhibit DNA damage responses, (2) increase telomerase expression, (3) inhibit telomere shortening; (4) promote cardiomyocyte survival/regeneration; (5) decelerate aging; and (6) extend lifespan (fig 1).  Together, this study suggests that pharmacological formulations encompassing “AP-1 or its activators, either alone or in combination with other drugs,”  may be used to improve cardiac function after myocardial infarction (fig. 2).  


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 AP-1 increase the expression of PNUTS/Telomerase?

Amount: $300#

# Research cooperation

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References

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

CitationBoominathan, L., Molecular therapy for Myocardial Infarction: AP-1 (Activator protein-1) inhibits DNA damage responses, induces telomerase expression, inhibits telomere shortening, and promotes cardiomyocyte survival after myocardial infarction, via up-regulation of PNUTS, 13/November/2018, 11.28 pm,  Genome-2-BioMedicine Discovery center (GBMD), http://genomediscovery.org

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