Anna Bakhtina and Gavin Pharaoh et al. recently published a new study in the high impact journal Nature Aging identifying that “Skeletal muscle mitochondrial interactome remodeling is linked to functional decline in aged female mice.”

Aging is a complex process involving many biological changes leading to loss of ability, chronic disease, and ultimately death. Mitochondria, which provide the energy for life, were among the first identified contributors to cellular aging. Aging mitochondria have many defects compared to young mitochondria leading to disruption in their vital functions such as energy production. To metabolize food and produce energy, many different proteins in the mitochondria must seamlessly interact with each other and work together. Before now, it was not possible to measure on a global scale how these proteins interact with each other. The interaction of all mitochondrial proteins is called the protein “interactome.”

In this study, the authors used an innovative chemical cross-linking proteomic technique to measure how the protein interactome of mitochondria changes with age in muscle. They paired this with measurements of functional capabilities of the mitochondria. They found that changes in the mitochondrial protein interactome contribute to the decline in mitochondrial function in aging. These changes include declines in specific complexes of the mitochondrial electron transport system, which generates the “charge” used to power the turbine-like ATP synthase. Mitochondrial protein interactomics provides a new powerful tool to identify age-related changes in mitochondria that contribute to functional decline.