(Philadelphia, PA) – Calcium transport into and out of mitochondria – the powerhouses of cells – is central to cellular energy production and cell death. To maintain the balance of calcium within these powerhouses, cells rely on a protein known as the mitochondrial sodium-calcium exchanger, or NCLX. Now, in new research, 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.

The discovery, described online April 8 in the journal Nature Metabolism, is the first to characterize the interaction of TMEM65 with NCLX in mitochondria. “TMEM65 is the first protein identified that is a bona fide interactor and regulator of NCLX,” explained John W. Elrod, PhD, W.W. Smith Chair in Cardiovascular Medicine and Founding Director of the Aging + Cardiovascular Discovery Center at the Lewis Katz School of Medicine and senior investigator on the new study. The discovery could help scientists design new therapeutic agents to combat calcium overload of mitochondria in conditions such as heart failure and Alzheimer’s disease.

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