Gavin Pharaoh et al. recently published a new study in the journal Geroscience identifying that “The mitochondrially targeted peptide elamipretide (SS-31) improves ADP sensitivity in aged mitochondria by increasing uptake through the adenine nucleotide translocator (ANT).”

 Mitochondria are like tiny cellular powerplants producing much of the energy for life. Decline in mitochondrial function play a pivotal role in aging and age-related diseases. One component affected by aging in mitochondria is disruption of the energy transfer and production pathway, which makes the mitochondria less able to respond to energetic demand. Mitochondria turn the food you eat into cellular energy by converting ADP to ATP. ANT is a transporter that exchanges ADP and ATP into the mitochondria during energy production. This transporter is critical for life and transports your body weight in ADP and ATP every day. During aging, mitochondrial energy production is less sensitive to ADP and requires more ADP to achieve the same energy production as young mitochondria.

Elamipretide is a small peptide that quickly improves aging muscle and heart function. The Marcinek Lab recently identified that elamipretide binds directly to ANT. The goal of this project was to test how Elamipretide binding affected the function of the ANT transporter in aging. The authors found that treatment with Elamipretide improved the sensitivity of old mitochondria to ADP by increased the uptake of ADP into mitochondria through the ANT transporter. Elamipretide treatment was associated with improved muscle and heart function.  This research supports the hypothesis that Elamipretide improves ANT function in aging and links ANT modification to improvement in physiological function. The rapid modification of ADP sensitivity is a promising path to develop interventions to restore muscle strength in aging.