Introduction: What they say:
A recent study from Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; and Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA shows that “The infarcted myocardium solicits GM-CSF for the detrimental oversupply of inflammatory leukocytes.” This study was published, in the 4 October 2017 issue of Journal of Experimental Medicine, by Prof Swirski FK, Anzai A 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 attenuating pathogenesis-associated with Myocardial infarction: Canagliflozin (Brand name: Invokana, Sulisent, Prominad, others), an anti-hyperglycemic medication used to treat type II diabetes, decreases GM-CSF (Granulocyte-macrophage colony-stimulating factor) expression, inhibits undue leucocyte activation and invasion, suppresses recruitment of inflammatory cells, inhibits left ventricular rupture, and promotes heart healing 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) out of 55 million deaths that occur every year, nearly 18.33 million deaths are due to cardiovascular causes; (3) the raise of death rate, due to cardiovascular disease, has increased from 123 lakhs in 1990 to 173 lakhs in 2013; (4) 85% of people over 80 years are susceptible to cardiovascular diseases;(5) in India, in 2004, 14.6 lakhs deaths (14% of total deaths) were due to ischemic heart disease; (6) the death due to cardiovascular disease is higher in low-to-middle income countries compared to developed countries; (7) the global economic cost spent in the treatment of cardiovascular disease in 2011 was little more than 10 billion US dollars; and (8) 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 excessive recruitment of leukocytes near the damaged myocardium. However, the mechanistic basis of which is far from clear.
Prof Swirski FK’s research team has shown recently that after the onset of Ischemia: (1) cardiac fibroblasts release excessive amount of GM-CSF; (2) GM-CSF promotes recruitment of inflammatory and proteolytic cells; (3) GM-CSF stimulates myeloid cells to attract neutrophils and monocytes, to the site of damaged myocardium; and (4) GM-CSF promotes left ventricular rupture. Evidently, mice null for GM-CSF do not recruit leukocytes near the damaged myocardium and they function well, suggesting that inhibition of GM-CSF or its receptor expression may attenuate pathogenesis-associated with myocardial infarction.
From Research Findings to Therapeutic Opportunity:
I had suggested earlier ( on 15/November/2018 at 10.02 pm and in other studies) that Canagliflozin may protect against myocardial dysfunction (https://genomediscovery.org/2018/11/the-known-anti-hyperglycemic-agent-empagliflozin-empa-may-safeguard-your-heart-against-cardiac-dysfunction-empagliflozin-empa-a-drug-used-in-the-treatment-of-tiidm/; &
Evidently, a very recent study from the the Stanford Center for Clinical Research, Department of Medicine, Stanford University School of Medicine, Stanford, CA, the George Institute for Global Health, University of New South Wales Sydney, the Royal North Shore Hospital and others shows that “Canagliflozin and Renal Outcomes in Type 2 Diabetes and Nephropathy.” This study was published, in the 14 April 2019 issue of of the prestigious journal N Engl J Med. (NEJM) (Impact factor: 79.258+) , by Prof. Mahaffey KW, Perkovic V, Brenner BM and others. In concordance with what I stated earlier, this study suggests that Canagliflozin lowers the risk of heart failure. However, the mechanism of action of this drug is not known yet.
This study provides mechanistic insights into how Canagliflozin may attenuate pathogenesis-associated with Myocardial infarction. Canagliflozin, by increasing the expression of its target genes, it may decrease the expression of GM-CSF (fig.1). Thereby, it may: (i) stall recruitment of inflammatory and proteolytic cells; (ii) inhibit accumulation of excessive amount of neutrophils and monocytes near the damaged myocardium; (iii) inhibit left ventricular rupture; (iv) suppress leukocyte supply chain; (v) control excessive inflammatory reaction; and (vi) improve myocardial function (fig 1).
Together, this study suggests that Canagliflozin, either alone or in combination with other compounds,” may be used to heal damaged cardiac tissue after myocardial infarction (fig. 1).
Attention: Since the entire text was misplaced, it was reposted on 19 May 2019 at 1.38 pm. We regret for the any inconvenience this may have caused.
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 Canagliflozin decreases the expression of GM-CSF, inhibits inflammatory leukocyte recruitment, and attenuates the pathogenesis-associated with myocardial infarction
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Citation: Boominathan, L., Molecular therapy for attenuating pathogenesis-associated with Myocardial infarction: Canagliflozin (Brand name: Invokana, Sulisent, Prominad, others), an anti-hyperglycemic medication used to treat type II diabetes, decreases GM-CSF (Granulocyte-macrophage colony-stimulating factor) expression, inhibits undue leucocyte activation and invasion, suppresses recruitment of inflammatory cells, inhibits left ventricular rupture, and promotes heart healing via up regulation of its target gene, 17/May/2019, 10.25 pm, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
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