MOTS-c attenuates cardiac dysfunction following high altitude exposure by promoting mitophagy.

Mice were kept in a decompression chamber set to 6000 meters for 10 days, then moved to a lower altitude of 400 meters for another 10 days. During that recovery period, some mice were given MOTS-c, a short peptide, while others were not. The researchers measured heart function, looked at mitochondria (the energy-producing parts of cells) in heart tissue, and checked levels of a protein called Pink1. They found that mice given MOTS-c had better heart function than those not given it, and that the peptide seemed to work by activating a pathway that clears out damaged mitochondria. When the researchers silenced Pink1, the beneficial effect disappeared. The paper also reports that people with high altitude heart disease and acute coronary syndrome had lower levels of MOTS-c in their blood, suggesting the peptide may be relevant to human heart problems.

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