Mitochondria-derived peptide MOTS-c alleviates hyperoxia-induced bronchopulmonary dysplasia in neonatal mice by activating Nrf2 pathway.

Newborn mice were placed in a chamber with 70% oxygen to mimic bronchopulmonary dysplasia, a lung condition that can affect premature babies. The researchers gave some of these mice MOTS-c, a peptide made of 16 amino acids, while others got no treatment. They also studied human umbilical vein cells in lab dishes, some of which were treated with MOTS-c and some with a drug that blocks a protein called Nrf2. Over the course of the study, they measured the mice's weight, looked at lung tissue under a microscope to see how the air sacs formed, and checked for signs of inflammation and oxidative stress, a type of cell damage. In the cells, they measured survival, death, and tube formation, which mimics blood vessel growth. The paper reports that mice given MOTS-c gained more weight, had less abnormal air sac enlargement, and showed fewer signs of inflammation and oxidative stress than untreated mice. The beneficial effects disappeared when Nrf2 was blocked, so the authors concluded that MOTS-c works through that pathway.

Read the paperView on PubMed(opens in a new tab)