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 of the journal Nature, by Prof Dimmler (Director, Center for Molecular Medicine), Boon RA, and others.
What we say:
On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: Why pollution is not good for your heart: Mechanistic and functional insights into how Pollutant Particulate matter (PM2.5) accelerates cardiac dysfunction: Particular matter (PM2.5) augments DNA damage responses, attenuates telomerase expression, promotes telomere shortening, and attenuates cardiomyocyte survival after myocardial infarction, via down regulation of PNUTS and others, 26/July/2020, 10.27 am
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:
The study presented here provides detailed mechanistic insights into how pollutant Particulate matter (PM2.5) promotes myocardial dysfunction.
Pollutant Particulate matter (PM2.5), by increasing the expression of its target genes, it may decrease the expression of cardiomyocyte survival protein PNUTS and others(fig.1) . Thereby, it may: (1) enhance DNA damage responses, (2) decrease telomerase expression, (3) promote telomere shortening; (4) decrease cardiomyocyte survival/regeneration; (5) accelerate cardiac ageing; (6) promote myocardial infarction or myocardial dysfunction; and (7) cardiac failure (fig 1).
Together, it is known for decades that pollutant Particulate matter (PM2.5) promotes heart attack and cardiac failure. However, the mechanistic basis of which remains largely unclear up until now. The study presented here, for the first time, provides plausible explanation and mechanistic and functional insights into how pollutant Particulate matter (PM2.5) may enhance the risk of cardiac dysfunction.
Thus, by avoiding inhaling pollutant Particulate matter (PM2.5), one may prevent ageing-associated (or, stress-associated) decline in cardiac function and cardiac failure (fig. 2). Together, this study provides, for the first time, mechanistic and functional insights into how pollutant particular matter (PM2.5) may promote or aggravate cardiac dysfunction and heart failure in the long-term (figs. 1-4).
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 does pollutant Particulate matter (PM2.5) decrease the expression of PNUTS/Telomerase?
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Citation: Boominathan, L., Why pollution is bad for your heart: Mechanistic and functional insights into how Pollutant Particular matter (PM2.5) accelerates cardiac dysfunction: Particular matter (PM2.5) augments DNA damage responses, attenuates telomerase expression, promotes telomere shortening, and attenuates cardiomyocyte survival after myocardial infarction, via down regulation of PNUTS and others, 26/July/2020, 10.45 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
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