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 Metabolic diseases: Combination of Amlodipine and Atorvastatin, a calcium channel blocker and an HMG-CoA reductase inhibitor, respectively, inhibits DNA damage responses, induces 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 reveals, for the first time, the previously known drugs’ unknown mechanism of action.
Atorvastatin (trade name: Lipitor/Atorva), an HMG-CoA reductase inhibitor and a lipid-lowering drug, is primarily used in the treatment of Cardiovascular disease; and is one of the best selling drugs in the US whose sales had crossed $125 billion from 1996-2012. Here, I present data that suggests that Atorvastatin, in combination with the anti-hypertensive drug and the calcium channel blocker Amlodipine, may function as a cardioprotective agent.
The Combination of Amlodipine and Atorvastatin, 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) promote insulin sensitivity; (6) decelerate ageing; and (7) extend life span (fig. 1).
Thus, by treating myocardial patients with the Combinatorial drug encompassing Amlodipine and Atorvastatin, one may prevent ageing-associated (or, stress-associated) decline in cardiac function. Together, this study suggests that pharmacological formulations encompassing “Amlodipine and Atorvastatin or their analogues” may be used to improve cardiac function, insulin sensitivity, hypertension, and lipid levels after myocardial infarction (fig.1).
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 the Combinatorial drug encompassing Amlodipine and Atorvastatin increases the expression of PNUTS and Telomerase
# Research cooperation
For purchase and payment details, you may reach us at email@example.com
Citation: Boominathan, L., Molecular therapy for Metabolic diseases: Combination of Amlodipine and Atorvastatin, a calcium channel blocker and an HMG-CoA reductase inhibitor, respectively, inhibits DNA damage responses, induces telomerase expression, inhibits telomere shortening, and promotes cardiomyocyte survival after myocardial infarction via up-regulation of PNUTS, 20/February/2017, 2.12 pm, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
Courtesy: When you cite drop us a line at firstname.lastname@example.org