Ribonucleic acid-based therapy protects against and promotes functional recovery after Myocardial Infarction:  LncRNA Mirt2 inhibits DNA damage responses, induces telomerase expression, inhibits telomere shortening, and promotes cardiomyocyte survival after myocardial infarction, via up-regulation of its target gene, 6/July/2019, 10.41 pm

Little RNA can save your heart from failing: Ribonucleic acid-based therapy for cardiomyocyte proliferation and heart regeneration: LncRNA Mirt2 (Long non-coding RNA myocardial infarction associated transcript 2) decreases tumor suppressor MiR-128 and cyclin-dependent kinase inhibitor p27 expression, increases SUZ12 expression, increases Cyclin E and CDK2 expression, promotes proliferation/re-entry of postnatal/adult cardiomyocytes, attenuates fibrosis, ameliorates cardiac dysfunction, and promotes heart repair in response to myocardial infarction, via up-regulation of its target gene, 6/July/2019, 10.25 pm
July 6, 2019
Little RNA can save you from cardiac hypertrophy and fibrosis: Intracardiac injection of LncRNA Mirt2 protects against cardiac hypertrophy and fibrosis: Intracardiac  injection of LncRNA Mirt2 (Long non-coding RNA myocardial infarction associated transcript 2) decreases MiR-29 expression, activates wnt- signaling and its components GSK3B, ICAT/CTNNBIP1, HBP1, and GLIS2, attenuates pathologic hypertrophy, inhibits fibrosis of the heart tissue, and improves cardiac function, via upregulation of its target gene, 6/July/2019, 11.14 pm
July 6, 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, 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: Ribonucleic acid-based therapy protects against and promotes functional recovery after Myocardial Infarction:  LncRNA Mirt2 inhibits DNA damage responses, induces telomerase expression, inhibits telomere shortening, and promotes cardiomyocyte survival after myocardial infarction, via up-regulation of its target gene

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 suggests, for the first time, that Intracardiac/epicardial injection of LncRNA Mirt2, 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.LncRNA Mirt2 functions as a Cardioprotective agent. LncRNA Mirt2 induces the expression of PNUTS and Telomerase to prevent myocardial infarction and promote Cardiac regeneration/survival (Updated on 6/July/2019, 10.41 pm)

Figure 2.  LncRNA Mirt2  functions as a cardioprotective agent through induction of PNUTS (Updated on 6/July/2019, 10.41 pm)

Figure 1.LncRNA Mirt2 functions as a Cardioprotective agent. LncRNA Mirt2 induces the expression of PNUTS and Telomerase to prevent myocardial infarction and promote Cardiac regeneration/survival

Figure 2.  LncRNA Mirt2  functions as a cardioprotective agent through induction of PNUTS

Thus, by injecting LncRNA Mirt2 into the myocardium of aged cardiac patients, one may prevent ageing-associated (or, stress-associated) decline in cardiac function. Together, this study suggests, for the first time, that pharmacological formulations encompassing “LncRNA Mirt2 or its inducers, 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 LncRNA Mirt2 increase 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/

Citations:

  1. Boominathan, L., Ribonucleic acid-based therapy protects against and promotes functional recovery after Myocardial Infarction:  LncRNA Mirt2 inhibits DNA damage responses, induces telomerase expression, inhibits telomere shortening, and promotes cardiomyocyte survival after myocardial infarction, via up-regulation of its target gene, 22/April/2019, 10.10 pm,  Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
  2. Boominathan, L., Ribonucleic acid-based therapy protects against and promotes functional recovery after Myocardial Infarction:  LncRNA Mirt2 inhibits DNA damage responses, induces telomerase expression, inhibits telomere shortening, and promotes cardiomyocyte survival after myocardial infarction, via up-regulation of its target gene, 6/July/2019, 10.41 pm,  Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org [Reposted again with up-to-date information]

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