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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 the journal Nature,  by Profs. Stefanie Dimmeler (Director, Center for Molecular Medicine), Reinier A 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 regenerative cardiovascular therapy:  MUC1-C inhibits DNA damage responses, induces telomerase expression, inhibits telomere shortening, and promotes cardiomyocyte proliferation, regeneration, and survival after myocardial infarction, via up-regulation of its target gene, 10/February/2021, 10.27 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

This study suggests, for the first time, that MUC1-C (MUC1{Mucin 1, cell surface associated (MUC1)} C-terminal subunit (MUC1C), also known as polymorphic epithelial mucin (PEM) or epithelial membrane antigen or EMA, could protect against myocardial dysfunction. 

MUC1-C, by increasing the expression of its target genes, it could 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/proliferation; (5) decelerate aging; and (6) extend lifespan (fig 1). 

Figure 1. MUC1-C  functions as a Cardioprotective agent. MUC1-C  prevents myocardial dysfunction and promotes cardiac regeneration/survival through induction of PNUTS, Telomerase and stem cell factors. 
Figure 2. MUC1-C functions as a cardioprotective agent through induction of PNUTS.
Figure 3. While it had been shown earlier that increased expression of PNUTS protects against myocardial dysfunction, this study suggests that MUC1-C may promote cardiac repair and protect against cardiac ageing and myocardial infarction through induction of PNUTS, telomerase and other genes.

Thus, by treating aged cardiac patients with MUC1-C or its inducers, one may prevent ageing-associated (or, stress-associated) decline in cardiac function. Together, this study suggests, for the first time, that pharmacological formulations encompassing “MUC1-C or its inducers or its functional or mechanistic equivalents, either alone or in combination with other cardio protective drugs, may be used to protect against myocardial infarction or improve cardiac function after myocardial infarction (figs. 1-3). 


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 MUC1-C 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 regenerative cardiovascular therapy:  MUC1-C inhibits DNA damage responses, induces telomerase expression, inhibits telomere shortening, and promotes cardiomyocyte proliferation, regeneration, and survival after myocardial infarction, via up-regulation of its target gene, 10/February/2021, 10.27 pm, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

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