Why cigarette smoking is not good for your heart: Mechanistic  and functional insights into how cigarette smoking accelerates cardiac dysfunction: Cigarette smoking augments DNA damage responses, attenuates telomerase expression, promotes telomere shortening, and attenuates cardiomyocyte survival after myocardial infarction, via down regulation of PNUTS and others, 28/August/2019, 1.55 pm

Consumption of olive oil can lengthen lifespan: Oleic acid-based anti-ageing and Lifespan extension therapy:  Oleic acid, the main constituent of olive oil, increases CHIP levels, increases monoubiquitylation of insulin receptor (INSR), decreases INSR protein levels and enhances lifespan, via down regulation of its target gene, 26/August/2019, 3.07 pm
August 26, 2019
Polypill to protect against cardiovascular dysfunction, including cardiac hypertrophy and fibrosis: A four-component Polypill consisting of Hydrochlorothiazide (12·5 mg), Aspirin (81 mg), Atorvastatin (20 mg), and Enalapril (5 mg) or Valsartan (40 mg) [Polypill-HAAE/HAAV] decreases MiR-29 expression, activates wnt- signaling and its components GSK3B, ICAT/CTNNBIP1, HBP1, and GLIS2, attenuates pathologic hypertrophy, inhibits fibrosis of the heart tissue, and improves cardiac function, via up regulation of its target gene, 30/August/2019, 12.03 am
August 29, 2019
Show all

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 cigarette smoking is not good for your heart: Mechanistic  and functional insights into how cigarette smoking accelerates cardiac dysfunction: Cigarette smoking augments DNA damage responses, attenuates telomerase expression, promotes telomere shortening, and attenuates cardiomyocyte survival after myocardial infarction, via down regulation of PNUTS and others, 28/August/2019, 1.53 pm


[easy_payment currency=”USD”]

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

A study from the Channing Laboratory, Department of MedicineHarvard Medical School, Boston, USA and others shows that Relative and absolute excess risks of coronary heart disease among women who smoke cigarettes. This study was published, in the19 November 1987 issue of of the prestigious journal N Engl J Med (Impact factor: 79+)by  Prof. Charles Hennekens H Willett and others. This study suggests that Cigarette smoking is associated with the risk of fatal coronary heart disease. However, the precise mechanism of action cigarette smoking remains largely unclear up until now. 

The study presented here substantiates and supports the aforementioned study’s’ claim, and others, by providing detailed mechanistic insights into how Cigarette smoking promotes myocardial dysfunction. 

Cigarette smoking, 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). 

Figure 1.  Mechanistic insights into how Cigarette smoking inhibits the expression of cardiac-survival protein PNUTS and others. And, thereby, promoting  cardiac ageing, myocardial infarction, while preventing cardiac regeneration/survival, resulting in cardiac failure.

Figure 2. Cigarette smoking may promote cardiac failure in cigarette smokers or myocardial patients through down regulation of PNUTS.

Figure 3. Cigarette smoking may promote cardiac ageing and attenuate cardiac function through down regulation of PNUTS. Thus, cigarette smokers are more prone to myocardial dysfunction compared to non-smoker population.

Figure 4.  While it had been shown that  in vivo silencing or genetic deletion of miR-34a  augments the expression of PNUTS, reduces cell death and fibrosis, and ameliorates functional recovery after acute myocardial infarction, the study presented here suggests, for the first time, that,  cigarette smoking decreases the expression of PNUTS, and promotes cardiac dysfunction. And, thereby, it makes cigarette smokers more susceptible  to coronary heart disease.

Figure 5. While it had been shown that cigarette smoking makes cigarette smokers more susceptible  to coronary heart disease,  the study presented here suggests, for the first time, that,  cigarette smoking decreases the expression of PNUTS, and promotes cardiac dysfunction. And, thereby, it makes cigarette smokers more susceptible  to coronary heart disease.

Together, it is known for decades that Cigarette smoking 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 Cigarette smoking may enhance the risk of cardiac dysfunction.

Thus, by avoiding smoking cigarette or being exposed to cigarette smoking (secondary smoking), 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 smoking cigarette  may promote or aggravate cardiac dysfunction and heart failure in the long-term (figs. 4-5).  


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 cigarette smoking decrease the expression of PNUTS/Telomerase?

Amount: $00#

# Research cooperation

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


References

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

CitationBoominathan, L., Why cigarette smoking is not good for your heart: Mechanistic  and functional insights into how cigarette smoking accelerates cardiac dysfunction: Cigarette smoking augments DNA damage responses, attenuates telomerase expression, promotes telomere shortening, and attenuates cardiomyocyte survival after myocardial infarction, via down regulation of PNUTS and others, 28/August/2019, 1.55 pm,  Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

Courtesy: When you cite drop us a line at admin@genomediscovery.org

Comments are closed.