New research links cell death during cardiac events to calcium overload

After discovering that CaM kinase II enzymes increase with cardiac events and lead to heart cell death, researchers from the University of Iowa have discovered new ways to inhibit these enzymes, potentially preventing further damage to heart cells and creating new treatment options for heart disease. Because heart cells aren't thought to easily regenerate, preventing or postponing damage onset can be a vital part of treatment.

Mitochondria provide energy to cells. During cardiac events, a mitochondrion may undergo a calcium overload and begin to leak, leading to death in cells that can't get enough energy - eventually spurring heart failure.

Researchers were able to inhibit CaM kinase II in genetically modified mice, stopping calcium overloads and preventing damage to heart cells.

The results of the study, published in Nature, could be used to improve treatment options for individuals with cardiovascular disease (CVD). At present, patients can buy Lipitor to address a range of heart ailments related to CVD, and other medications can be found at cost-competitive prices from a Canadian internet pharmacy. Exercise and diet have also been shown to reduce the risk of certain heart conditions.

"Because mitochondria also play important roles in other diseases in brain and skeletal muscle, for example, our findings could also have broad implications for understanding and treating non-cardiac diseases," said lead study author Mark Anderson, M.D., Ph.D., head of internal medicine at the UI Carver College of Medicine.