Introduction: What they say
A recent study from the Stem Cell Aging Group, Centro Nacional de Investigaciones Cardiovasculares, E-28029 Madrid, Spain shows that “Bmi1 limits dilated cardiomyopathy and heart failure by inhibiting cardiac senescence.” This study was published in the online journal 9 March 2015 issue of Nature Communications by Prof Gonzalez, Gonzalez-Valdes and others.
What we say:
On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: Cardiac rejuvenation therapy: AML-3 (Cbfa1/Runx2) suppresses tumor suppressor INK4a/p16 expression, and inhibits dilated cardiomyopathy and heart failure via up regulation of its target gene
From the Significance of the study to Public health relevance:
Given that: (1) cardiovascular disease is the leading cause of death worldwide; (2) Dilated cardiomyopathy is the leading cause of Heart failure; (3) the raise of death rate, due to cardiovascular disease, has increased from 12.3 million in 1990 to 17.3 million in 2013; (4) 13% of cardiovascular disease occur due to uncontrolled high blood pressure; (5) in India, in 2004, 14.6 lakhs deaths (14% of total deaths) were due to ischemic heart disease; (6) 85% of people over 80 years are susceptible to cardiovascular diseases; (7) the global economic cost spent in the treatment of cardiovascular disease in 2011 was little more than 10 billion US dollars; (8) the death due to cardiovascular disease is higher in low-to-middle income countries compared to developed countries; and (9) 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 cure to diseases, as mentioned above, leading to cardiovascular disease; (ii) a way to induce regeneration of adult cardiomyocytes that were lost in Myocardial patients; (iii) 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 AML-3/ Cbfa1/Runx2, by increasing the expression of its target gene, it may suppress the expression of tumor suppressor and the ageing marker INK4a/p16 (figure 1).
Thereby, it may: (1) inhibit cardiac senescence; (2) increase of regenerative potential in aged tissues; and (3) improve ventricular dimensions and contractility. Thus, (1) by treating myocardial patients with AML-3/ Cbfa1/Runx2 activators, one may prevent Dilated cardiomyopathy and ageing-associated (or, stress-associated) decline in cardiac function; and (2) pharmacological formulations encompassing “AML-3/ Cbfa1/Runx2 activators or their analogues or AML-3/ Cbfa1/Runx2 activators plus any of the known drugs that inhibit cardiomyopathy“ may be used to inhibit dilated cardiomyopathy and heart failure (figure 1).
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 AML-3/ Cbfa1/Runx2 suppresses the expression of tumor suppressor INK4a/p16.
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Citation: Boominathan, L., Cardiac rejuvenation therapy: AML-3 (Cbfa1/Runx2) suppresses tumor suppressor INK4a/p16 expression, and inhibits dilated cardiomyopathy and heart failure via up regulation of its target gene, 3/January/2017, 2.09 pm, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
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