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: IGFBP2 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, 8/February/2021, 9.26 am
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 IGFBP2 (Insulin Like Growth Factor Binding Protein 2) could protect against myocardial dysfunction.
IGFBP2, 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).
Thus, by treating aged cardiac patients with IGFBP2 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 “IGFBP2 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 FOXK2 increase the expression of PNUTS/Telomerase?
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Citation: Boominathan, L., Molecular regenerative cardiovascular therapy: IGFBP2 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, 8/February/2021, 9.25 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
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