There appears to be a study praising the health benefits of coffee published every other week.
Over recent years, researchers have concluded that caffeine protects against diabetes, heart failure, and stroke.
Higher levels of coffee consumption have also been linked with a lower risk of mortality.
Still, as the evidence mounts in support of caffeine’s health benefits, the mechanism behind its protective powers is still not completely understood.
Scientists from Heinrich-Heine-University and the IUF-Leibniz Research Institute for Environmental Medicine in Düsseldorf, Germany, recently set out to identify the cellular pathways involved in caffeine’s heart-protective ability.
The role of mitochondria
In earlier experiments, the authors of the new study found that caffeine levels equivalent to around four cups of coffee improved the function of endothelial cells, which line the inside of blood vessels.
They also revealed that the benefits that caffeine imparted seemed to involve mitochondria. These, as everyone is well aware, are commonly referred to as the powerhouses of the cell — a description so well known it has achieved meme status.
Mitochondria won their title because, within their membranes, adenosine triphosphate — which is the energy currency of life — is produced.
In their latest study, they identified a new player within mitochondria that appears to be relevant to caffeine’s protective effect: p27. Their findings were published in the journal PLOS Biology.
First identified as an inhibitor of the cell cycle, p27 is an enzyme that normally slows cell division.
The researchers — led by Judith Haendeler and Joachim Altschmied — found that caffeine caused p27 to move into mitochondria. Once within these organelles, it triggered tasks vital for the repair of heart muscle following a heart attack.
These tasks include promoting migration of endothelial cells and protecting heart muscle cells from cell death, also known as apoptosis. p27 also sparked activity in fibroblasts, or cells that synthesize certain structural components of tissues. Caffeine encourages fibroblasts to produce essential contractile fibers.
Further to these findings, the scientists found that caffeine protected against heart damage in prediabetic, older, and obese mice. They have high hopes for the future implications of these results.
Haendeler concludes, “These results should lead to better strategies for protecting heart muscle from damage, including consideration of coffee consumption or caffeine as an additional dietary factor in the elderly population.”
“Furthermore,” she says, “enhancing mitochondrial p27 could serve as a potential therapeutic strategy not only in cardiovascular diseases but also in improving healthspan.”
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