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A Relaxin(g)-way to say no to cardiac diseases: Relaxin-based therapy for attenuating pathogenesis-associated with Myocardial infarction: Relaxin, a reproductive hormone,  decreases IRF3 (Interferon regulatory transcription factor-3), GM-CSF (Granulocyte-macrophage colony-stimulating factor) and GRK2(G protein-coupled receptor kinase) expression, inhibits undue leucocyte activation and invasion, suppresses recruitment of inflammatory cells, inhibits ventricular dilation, and promotes heart repair and survival, via up-regulation of its target gene, 18/August/2018, 1.11 am

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Introduction: What they say:

A recent study from Department of Systems Biology, Harvard Medical School, Boston, Massachusetts, USA; and Cardiovascular Research Center, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA shows that “IRF3 and type I interferons fuel a fatal response to myocardial infarction.” This study was published, in the 6 November 2017 issue of Journal Nature Medicine (One of the best journals in Bio-Medicine with an impact factor of 29.886), by Prof Ralph Weissleder, Kevin R King, and others.


What we say:

On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: A Relaxin(g)-way to say no to cardiac diseases: Relaxin-based therapy for attenuating pathogenesis-associated with Myocardial infarction: Relaxin, a reproductive hormone,  decreases IRF3 (Interferon regulatory transcription factor-3), GM-CSF (Granulocyte-macrophage colony-stimulating factor) and GRK2(G protein-coupled receptor kinase) expression, inhibits undue leucocyte activation and invasion, suppresses recruitment of inflammatory cells, inhibits ventricular dilation, and promotes heart repair and survival, 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) 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 from 2030 onwards, 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.


What is known?

It is known for years that myocardial infarction results in activation of inflammatory mediators and excessive recruitment of leukocytes near the damaged myocardium. However, the mechanistic basis of which is far from clear.

Prof Ralph Weissleder FK’s research team has shown recently that: (1) mice null for IRF3 and IFNAR have improved survival after myocardial infarction; (2) inhibition of IRF3 signalling: a) decreases the expression of cardiac inflammatory mediators; b) prevents inflammatory cell infiltration of the myocardium; c) reduces ventricular enlargement; and d) ameliorates cardiac function; and (3) treating mice with IFNAR-neutralizing antibody alter myocardial infarction: a) attenuates interferon response; b) improves left ventricular dysfunction; and (c) promotes survival, suggesting that inhibition of IRF3 or IFNAR expression may: (1) attenuate pathogenesis after myocardial infarction; (2) aid post-myocardial infarction protection; and (3) stall myocardial infarction from progressing to heart failure.


From Research Findings to Therapeutic Opportunity:

This study suggests, for the first time, that the reproductive hormone Relaxin may in attenuating pathogenesis-associated with Myocardial infarction. 

Relaxin, a protein hormone, has been shown to play a role in the control of diabetes, obesity, and cardiac diseases. However, the mechanism of action remains unclear.

Relaxin, by increasing the expression of its target genes, it may decrease the expression of IRF3, GRK2 and GM-CSF (fig.1). Thereby, it may: (i) inhibit the expression of inflammatory mediators; (ii) stall inflammatory cell infiltration; (iii) inhibit ventricular dilation; (iv) improve cardiac function and survival; and (v) inhibit inflammatory reaction post-MI. Together, this study suggests that relaxin-based therapy may be used to heal damaged cardiac tissue after myocardial infarction

Figure 1. Mechanistic insights into how Relaxin may function as a cardioprotective agent. Relaxin may decrease the expression of IRF3, GRK2, and-GM-CSF and other genes that promote pathogenesis-associated with myocardial infarction.

Figure 2. Relaxin suppresses pathogenesis associated myocardial infarction through down-regulation of GM-CSF, GRK2, and IRF3.


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 Relaxin decreases the expression of IRF3, GRK2, and IRF3, inhibits inflammatory leukocyte recruitment, and attenuates the pathogenesis associated with myocardial infarction

Amount: $1, 500 #

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References:

Web:http://genomediscovery.org or http://newbioideas.com/

Citation: Boominathan, L., A Relaxin(g)-way to say no to cardiac diseases: Relaxin-based therapy for attenuating pathogenesis-associated with Myocardial infarction: Relaxin, a reproductive hormone,  decreases IRF3 (Interferon regulatory transcription factor-3), GM-CSF (Granulocyte-macrophage colony-stimulating factor) and GRK2(G protein-coupled receptor kinase) expression, inhibits undue leucocyte activation and invasion, suppresses recruitment of inflammatory cells, inhibits ventricular dilation, and promotes heart repair and survival, via up-regulation of its target gene, 18/August/2018, 1.11 am, Genome-2-BioMedicine Discovery center (GBMD), http://genomediscovery.org

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