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: Sitagliptin, a Dipeptidyl peptidase-4 (DPP-4) inhibitor and an anti-hyperglycemic drug, 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:
This study provides mechanistic insights into how Sitagliptin, the Dipeptidyl peptidase-4 (DPP-4) inhibitor and an anti-hyperglycemic drug, may promote cardiac survival and regeneration.
Sitagliptin, by increasing 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; and (4) promote cardiomyocyte survival/regeneration (figure 1).
Thus, by treating myocardial patients with Sitagliptin (figure 1), one may prevent ageing-associated (or, stress-associated) decline in cardiac function. Given that myocardial complications follow diabetes, it may be an agent of choice in the treatment and management of TIIDM.
Together, this study suggests that pharmacological formulations encompassing “Sitagliptin or its analogues or Sitagliptin 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 Sitagliptin increases the expression of PNUTS and Telomerase
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Citation: Boominathan, L., Molecular therapy for Myocardial Infarction: Sitagliptin, a Dipeptidyl peptidase-4 (DPP-4) inhibitor and an anti-hyperglycemic drug, inhibits DNA damage responses, increases telomerase expression, inhibits telomere shortening, and promotes cardiomyocyte survival after myocardial infarction via up-regulation of PNUTS, 2/January/2017, 10.35 pm, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
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