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

What this study reported

Reported that simulated high-altitude exposure in mice was followed by persistent cardiac and mitochondrial dysfunction and lower cardiac MOTS-c during a 10-day de-acclimatization period at lower altitude. Found that administered MOTS-c during de-acclimatization was associated with less cardiac dysfunction in these mice, with activation of the Pink1/Parkin pathway and greater mitophagy, and that silencing Pink1 abolished the association. Measured lower circulating MOTS-c in patients with high altitude heart disease and in patients with acute coronary syndrome.

Limitations

Single mouse strain and males only with group sizes not reported in the abstract, a simulated decompression-chamber model rather than field exposure, and the human component is a small cross-sectional comparison of circulating levels without reported sample sizes.