MOTS-c attenuates hyperoxia-induced neonatal cardiac injury by inhibiting oxeiptosis via maintaining the KEAP1-PGAM5 interaction.

Newborn mice were placed in chambers with 85% oxygen to model the heart damage that high oxygen can cause in human newborns. Some of these mice were given MOTS-c, a peptide made by mitochondria, while others were not. The researchers also grew rat heart cells in high oxygen in the lab and treated some of those with MOTS-c. They measured heart size, scar tissue, and pumping function in the mice, and looked at cell death pathways in both the mice and the cells. The paper reports that mice given MOTS-c had less heart thickening and scarring and better heart function than the untreated mice, and that the compound appeared to block a specific type of cell death triggered by oxygen damage.

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