A team of researchers from the Department of Surgery at the University of South Florida (United States) has made a key discovery about why we become more susceptible to heart disease as we age.
The human body, especially the heart, relies on mitochondria, the part of the cell responsible for producing energy to maintain organ function. The protein, Sesn2, is found inside the mitochondria and plays a critical role in protecting the heart against stress.
According to their findings, published in the journal Redox Biology, Sesn2 levels decrease over time, which weakens the heart and can cause it to lose function. The study points out that an insufficient level of Sesn2 is the reason why the elderly have a higher risk of heart attack and other heart complications. This indicates that stabilizing protein could be the answer to maintaining a healthy heart.
It is common for people who have suffered cardiac arrest to have a stent inserted into a blood vessel to relieve the blockage or to be prescribed medications designed to prevent blood clots. Although they can offer quick relief, these treatments can cause further damage to the heart. There are currently no known treatments available to prevent these possible side effects. The research group found that targeting Sesn2 can maintain the functional integrity of mitochondria, compensating for such complications.
Through biochemical analysis and high-powered microscopes, they were able to see that Sesn2 deficiency caused cell death in old mice, inducing a heart attack. The researchers are now in the process of confirming their findings on human hearts. Thus, they hope to have those results available in the next two years.
