12 January - 20 June 2016

Caffeine, an amount found in 4 cups of coffee, can protect heart cells from damage

German scientists in PLOS Biology describe how caffeine enhances the function of heart cells and protects them from damage. Previous research has found an association between caffeine and multiple diseases including heart disease, stroke and type II diabetes, however the protective mechanisms remain unclear.

German scientists in PLOS Biology describe how caffeine enhances the function of heart cells and protects them from damage. Previous research has found an association between caffeine and multiple diseases including heart disease, stroke and type II diabetes, however the protective mechanisms remain unclear.  The beneficial effects of caffeine have been found to be dose dependent, with “4 cups or more per day resulted in a further reduced risk for adverse events when compared to lower coffee consumption.”  Four cups of coffee per day have been found to lead to a blood concentration of around 30 µM caffeine in humans.  In this current mouse study Altschmied et al. used 50 µM, stating that this concentration of caffeine in the drinking water of mice, results in approximately 30 – 50 µM in the serum of the animals.

This current study builds on previous research by Altschmied et al. which found that caffeine increases the functional capacity of endothelial cells that line blood vessels.  Caffeine increases the protein p27 present in mitrochondria cells, a major cell in the heart, protecting the heart muscle cells from cell death.  In the current study the team analysed the potential role of p27 in the major cell types of the heart and investigated the protective effect of caffeine in pre-diabetic, obese mice and in aged mice.

The team initially investigated the impact of 50 µM caffeine on endothelial cell migration in the presence of adenosine receptors 2A and 2B blockers SCH442416 and GS6201.  They report that “neither inhibition adenosine receptor 2A nor 2B changed the ability of 50 µM caffeine to induce migration in human primary endothelial cells”.  They also investigated whether p27 is found in the mitochondria, confirming that treatment significantly increased mitochondrial p27 and is localised in mitochondria.  Caffeine was also found to induce the movement of p27 into mitochondria, setting off a beneficial chain of events, promoting migration of endothelial cells, protecting heart muscle from cell death and triggering of the conversion of fibroblast into cells containing contractile fibres, all of which are crucial for repair of heart muscle after myocardial infarction.  Using mice that were deficient in p27 the team confirmed this finding.  The mice were found to have impaired mitochondrial function that did not improve with caffeine.

A common effect of the ageing process is reduced mitochondrial respiratory capacity (via a complex sequence of biochemical events).  22-month-old mice were treated for 10 days with caffeine, the equivalent found in 4-5 cups of coffee, with the finding that the caffeine increased mitochondrial respiration to the levels observed in 6 moth old mice.  The researchers state that “the analysis of cardiac mitochondria from old mice showed a roughly 2-fold increase in mitochondrial p27 content after 10 days of caffeine, demonstrating that caffeine-induced improved respiration is paralleled by an increase in mitochondrial p27”.  As obesity and type 2 diabetes have been found to be associated with mitochondrial dysfunction, the researchers investigated obese and prediabetic state mice, finding that compared to a control group, the mice that received caffeine in their drinking water had improved ventricular wall thickness with caffeine significantly increasing p27 in the mitochondrial of the mice.

In conclusion the authors state “our results indicate a new mode of action for caffeine, one that promotes protection and repair of heart muscle through the action of p27.  These results should lead to strategies for protecting heart muscle from damage, including consideration of coffee consumption or caffeine as an additional dietary factor in the elderly population.  Furthermore, enhancing mitochondrial p27 could serve as a potential therapeutic strategy not only in cardiovascular diseases but also in improving lifespan”.

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