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 Myocardial Infarction: PDLIM1/2 (PDZ And LIM Domain 1) inhibits DNA damage responses, increases 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 provides mechanistic insight into how PDLIM1/2 may promote cardiac survival and regeneration.
PDLIM1/2 (figure 1), by increasing the expression of its target genes, it may increase the expression of PNUTS and the cellular immortality gene Telomerase. Thereby, it may: (1) inhibit DNA damage responses, (2) increase Telomerase expression; (3) inhibit telomere shortening; and (4) promote cardiomyocyte survival/regeneration (figure 1).
Figure 1. Mechanistic insights into how PDLIM1/2 induce the expression PNUTS and Telomerase to promote Cardiac regeneration and survival
Thus, by treating myocardial patients with PDLIM1/2 activators (figure 1), one may prevent ageing-associated (or, stress-associated) decline in cardiac function.
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Together, this study suggests that pharmacological formulations encompassing “PDLIM1/2 activators or PDLIM1/2 activators plus any of the known drugs that improve myocardial function” may be used to improve cardiac function after myocardial infarction.
Details of the research findings:
Idea Proposed/Formulated (with experimental evidence) by:
Dr L Boominathan Ph.D.
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Undisclosed mechanistic information: How PDLIM1/2 increase the expression of PNUTS and Telomerase
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References:
Web:http://genomediscovery.org or http://newbioideas.com
Citation: Boominathan, L., Molecular therapy for Myocardial Infarction: PDLIM1/2 (PDZ And LIM Domain 1) inhibit DNA damage responses, increase telomerase expression, inhibit telomere shortening, and promote cardiomyocyte survival after myocardial infarction via up-regulation of PNUTS, 21/December/2016, 2.46 pm, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
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