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An omega-3 way to say no to Cardiomyopathy: PUFA-based therapy for Cardiomyopathy: ω-PUFAs (Docosahexaenoic acid (DHA) + Eicosapentaenoic acid (EPA)) decrease the expression of Sox6, restore the balance between slow- and fast-twitch myofiber proteins and alleviate Cardiomyopathy via up regulation of its target gene, 13/April/2018, 10.05 pm

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Introduction: What they say  

A study from the Department of Cardiology, Boston Children’s Hospital, Harvard Medical School, Boston, Massachusetts, USA; and Harvard Stem Cell Institute, Harvard University, Cambridge, Massachusetts, USA shows that Trbp regulates heart function through microRNA-mediated Sox6 repression.” This study was published, in the 2 June  2015 issue of the journal “Nature Genetics” (the number 1 research journal in Genetics with an impact factor of 29.648), by Prof. Da-Zhi Wang & Jian Ding, and others

Further, a recent study from the Population Health Research Institute, McMaster University and Hamilton Health Sciences, David Braley Research Bldg., Hamilton General Hospital, 237 Barton St. E., Hamilton, ON L8L 2X2, Canada shows that “Rivaroxaban with or without Aspirin in Stable Cardiovascular Disease.” This study was published, in the 27 August  2017 issue of the journal “N Engl J Med.” (the number 1 journal in “Clinical medicine” with an impact factor of 72.406), by Dr. Eikelboom, Stuart J. Connolly and others.


What we say:

On the foundation of these interesting findings, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: An omega-3 way to say no to Cardiomyopathy: PUFA-based therapy for Cardiomyopathy: ω-PUFAs (Docosahexaenoic acid (DHA) + Eicosapentaenoic acid (EPA)) decrease the expression of Sox6, restore the balance between slow- and fast-twitch myofiber proteins and alleviate Cardiomyopathy via up regulation of its target gene


From 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.


What is known?

A number of studies suggests that Cardiomyopathy is the result of altered gene expression of contractile proteins. Trbp, an RNA binding protein, has been shown to be required for normal functioning of heart contractions.

Prof Da-Zhi Wang’s research team has shown earlier that inactivation of Trbp in mice leads to progressive cardiomyopathy and heart failure. 


From research findings to Therapeutic opportunity: 

This study suggests  a PUFA (Polyunsaturated fatty acid)-based therapy for Cardiomyopathy.  ω-PUFAs (Docosahexaenoic acid (DHA) + Eicosapentaenoic acid (EPA) ) have recently been shown to shown to function as anti-hyperglycemic agents. However, the exact mechanism of action remains unclear. This study suggests, for the first time, that ω-PUFAs, by regulating  the expression of their target genes, they may: (1) decrease the expression of Sox6; (2) increase the expression of cardiac slow-twitch myofiber proteins; (3) decrease the expression of skeletal fast-twitch myofiber proteins;  (4) restore the balance between slow- and fast-twitch myofiber proteins; and (5) alleviate cardiomyopathy (fig. 1).

Figure 1. Mechanistic insights into how  ω-PUFAs function as cardioprotective agents. ω-PUFAs, by increasing the expression of their target genes, they may decrease the expression of Sox6. Thereby, they may increase cardiomyocyte proliferation, augment the number of beating cardiomyocytes, and attenuate cardiomyopathy

Figure 2. The chemical structure of ω-PUFAsω-PUFAs may attenuate diabetic cardiomyopathy and cardiac ageing through down regulation of Sox6.

Thus, pharmacological formulations encompassing ω-PUFAs (Docosahexaenoic acid (DHA) + Eicosapentaenoic acid (EPA) ) or their analogues, either alone or in combination with other drugs,” may be used to inhibit progressive cardiomyopathy and lethal heart failure.

Given the mechanism of  action of ω-PUFAs, medical practitioners and cardiologists may consider recommending their cardiac patients to take it, as it is being inexpensive and non-toxic compared to other cardioprotective drugs. 

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Details of the research findings:

Idea Proposed/Formulated byDr L Boominathan Ph.D.

Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/

Undisclosed mechanistic information: How ω-PUFAs inhibit the expression of Sox6.

#Research cooperation

Amount: $500#

For purchase and payment details, you may reach us at info@genomediscovery.org


References:

Web: http://genomediscovery.org

To citeBoominathan, L., An omega-3 way to say no to Cardiomyopathy: PUFA-based therapy for Cardiomyopathy: ω-PUFAs (Docosahexaenoic acid (DHA) + Eicosapentaenoic acid (EPA)) decrease the expression of Sox6, restore the balance between slow- and fast-twitch myofiber proteins and alleviate Cardiomyopathy via up regulation of its target gene, 13/April/2018, 10.05 pm,  Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

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