Molecular mechanistic insight into how Dapagliflozin (DAPA)  protects against and promotes functional recovery after Myocardial Infarction:  Dapagliflozin (DAPA) (trade name: Forxiga, Farxiga, others), a medication used to treat type II diabetes,  inhibits DNA damage responses, induces telomerase expression, inhibits telomere shortening, and promotes cardiomyocyte survival after myocardial infarction, via up-regulation of its target gene, 26/September/2019, 3.58 pm

Polypill for Cardioprotection: Polypill-HAAE/HAAV-based therapy for Cardiac repair and myocardial infarction: A four-component  Polypill-HAAE/HAAV consisting of Hydrochlorothiazide (12·5 mg), Aspirin (81 mg), Atorvastatin (20 mg), and Enalapril (5 mg)  or Valsartan (40 mg)  increases Agrin expression, activates Yap and ERK-mediated signaling,  replaces scar tissue with functional cardiomyocytes, and promotes cardiomyocyte regeneration and repair after myocardial infarction, via up-regulation of its target gene, 25/September/2019,  8.45 pm
September 25, 2019
Cardiovascular Polypill-LAAH attenuates pathogenesis-associated with Myocardial infarction and protects against myocardial dysfunction:   A four-component Polypill-LAAH consisting of Losartan(25 mg), Amlodipine (2.5 mg), Atorvastatin (10 mg), and Hydrochlorothiazide (12·5 mg)decreases IRF3, GM-CSF (Granulocyte-macrophage colony-stimulating factor) and GRK2(G protein-coupled receptor kinase) expression, inhibits undue leukocyte activation and invasion, suppresses recruitment of inflammatory cells, inhibits ventricular dilation, and promotes heart repair and survival, via up regulation of its target genes, 1/October/2019, 12.04 pm
October 1, 2019
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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 (Director, Center for Molecular Medicine), 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 mechanistic insight into how Dapagliflozin (DAPA)  protects against and promotes functional recovery after Myocardial Infarction:  Dapagliflozin (DAPA) (trade name: Forxiga, Farxiga, others), a medication used to treat type II diabetes,  inhibits DNA damage responses, induces telomerase expression, inhibits telomere shortening, and promotes cardiomyocyte survival after myocardial infarction, via up-regulation of its target gene, 26/September/2019, 3.58 pm


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

A study from the BHF Cardiovascular Research Centre, University of Glasgow, Glasgow, United Kingdom; the Cardiovascular Division and the TIMI Study Group, Brigham and Women’s Hospital and Harvard Medical School  and others shows that Dapagliflozin in Patients with Heart Failure and Reduced Ejection Fraction. This study was published, in the 19 September 2019 issue of of the prestigious journal N Engl J Med. (Impact factor: 7o +)by  Prof. Langkilde AM., MD., PhD., McMurray JJV, M.D.,  and others. This study suggests that those  patients who consumed Dapagliflozin (DAPA) are at reduced risk of  major cardiovascular events.  However, the precise mechanism of action of Dapagliflozin (DAPA) remains unclear. 

The study presented here substantiates and supports the aforementioned study’s’ claim, and of others, by providing detailed mechanistic insights into how Dapagliflozin (DAPA) attenuates and thereby protects against myocardial dysfunction, including cardiac hypertrophy, fibrosis of the myocardium, cardiac ageing and myocardial infarction.

This study provides, for the first time, mechanistic insights into how Dapagliflozin (DAPA) may protect against myocardial dysfunction. 

Dapagliflozin (DAPA), 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).  

Figure 1. Dapagliflozin (DAPA) functions as a Cardioprotective agent. Dapagliflozin (DAPA)  induces the expression of PNUTS and Telomerase to prevent myocardial infarction and promote Cardiac regeneration/survival .

Figure 2.  Dapagliflozin (DAPA)  functions as a cardioprotective agent through induction of PNUTS.

Figure 3 While it had been shown earlier that Dapagliflozin (DAPA) protects against myocardial dysfunction, its mechanism of action remains unclear. The study presented here suggests that Dapagliflozin (DAPA)  may promote cardiac repair and protect against cardiac ageing and myocardial infarction through induction of PNUTS, telomerase and other genes.

Figure 4. While it had been shown earlier that increased expression of PNUTS protects against myocardial dysfunction, this study suggests that Dapagliflozin (DAPA) may promote cardiac repair and protect against cardiac ageing and myocardial infarction through induction of PNUTS, telomerase and other genes.

Thus, by recommending aged cardiac patients to take Dapagliflozin (DAPA), one may prevent ageing-associated (or, stress-associated) decline in cardiac function. Together, this study suggests, for the first time, that pharmacological formulations encompassing “Dapagliflozin (DAPA) or its analogs or its functional or mechanistic equivalents, either alone or in combination with other drugs, may be used to protect against myocardial infarction or 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 Dapagliflozin (DAPA) increase the expression of PNUTS/Telomerase?

Amount: $ 1, 500 #

# Research cooperation

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References:

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

CitationBoominathan, L., Molecular mechanistic insight into how Dapagliflozin (DAPA)  protects against and promotes functional recovery after Myocardial Infarction:  Dapagliflozin (DAPA) (trade name: Forxiga, Farxiga, others), a medication used to treat type II diabetes,  inhibits DNA damage responses, induces telomerase expression, inhibits telomere shortening, and promotes cardiomyocyte survival after myocardial infarction, via up-regulation of its target gene, 26/September/2019, 3.58 pm,  Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

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