Discovery of mitochondrial protein opens path to therapeutic advances for heart and Alzheimer’s disease

Calcium transport into and out of mitochondria is central to cellular energy production and cell death. To maintain the balance of calcium within mitochondria, cells rely on a protein known as the mitochondrial sodium-calcium exchanger, or NCLX. Now, scientists at the Lewis Katz School of Medicine at Temple University have discovered a novel regulator of NCLX activity, a protein called TMEM65, which helps move calcium out of mitochondria, protecting against harmful calcium overload.