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Why high glucose is not good for your heart: Mechanistic insights into how glucose-rich foods may accelerate cardiac ageing: High glucose augments DNA damage responses, attenuates telomerase expression, promotes telomere shortening, and attenuates cardiomyocyte survival after myocardial infarction, via down regulation of PNUTS, 24/June/2018, 5.52 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: Why high glucose is not good for your heart: Mechanistic insights into how glucose-rich foods may accelerate cardiac ageing: High glucose augments DNA damage responses, attenuates telomerase expression, promotes telomere shortening, and attenuates cardiomyocyte survival after myocardial infarction, via down 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 suggests, for the first time, how high glucose levels, which is common in untreated diabetic condition,  may promote cardiac dysfunction.

Figure 1.  Mechanistic insights into how Glucose inhibits the expression of cardiac-survival protein PNUTS and Telomerase to prevent myocardial infarction and promote Cardiac regeneration/survival

Figure 2.  High glucose level may promote cardiac ageing and decelerate cardiac function  may through down regulation of PNUTS

High glucose, by increasing the expression of its target genes, it may decrease the expression of PNUTS (fig.1)Thereby, it may: (1) enhance DNA damage responses, (2) decrease telomerase expression, (3) promote telomere shortening; (4) decrease cardiomyocyte survival/regeneration; (5) accelerate ageing; and (6) extend life span (fig 1). 

Thus, by staying away from sugar-rich foods, one may prevent ageing-associated (or, stress-associated) decline in cardiac function. Together, this study provides, for the first time, mechanistic insights into how high glucose levels may promote cardiac dysfunction and cardiac ageing in the long-term (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 high glucose decrease the expression of PNUTS/Telomerase

Amount: $300#

# Research cooperation

For purchase and payment details, you may reach us at admin@genomediscovery.org


References

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

CitationBoominathan, L., Why high glucose is not good for your heart: Mechanistic insights into how glucose-rich foods may accelerate cardiac ageing: High glucose augments DNA damage responses, attenuates telomerase expression, promotes telomere shortening, and attenuates cardiomyocyte survival after myocardial infarction, via down regulation of PNUTS, 24/June/2018, 5.52 pm,  Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

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