A new study conducted by researchers from the University of Iowa on mice showed that the increased risk of death with heart attacks in diabetic patients could be due to activation of a vital heart enzyme which leads to the death of pacemaker cells and an irregular heart rate.
The death rates of diabetic adults with heart diseases are 2 to 4 times higher than adults without diabetes. The primary cause of death in diabetic patients in US population is myocardial infraction (heart attack).
The study published in the latest edition of the Journal of Clinical Investigation states that heart rhythm abnormalities caused due to the death of pacemaker cells is the cause of the heart attack deaths in diabetic mice, which involves a pathway where oxidized CaMKII (calcium/calmodulin-dependent protein kinase II) enzyme plays a major role. Researchers found elevated levels of oxidized CaMKII in the pace maker cells of diabetic mice than in non-diabetic mice. It was found that the levels of oxidation and cellular deaths were much more following a heart attack in diabetic mice.
This multifunctional protein kinase called CaMKII is activated by oxidative stress, which is caused by reactive oxygen species (ROS). These are oxygen containing chemically reactive molecules. Previous studies show that increased levels of ROS are produced as a product of cellular metabolism under diabetic conditions in various tissues, which results in cellular damage.
The blockage of oxidation-based activation of enzyme reduced the death of pacemaker cells and protected the mice from the heart attack deaths. So the researchers concluded that the increased levels of activated CaMKII could be a diabetic factor leading to heart attacks.