MNRR1 activation by nitazoxanide abrogates lipopolysaccharide-induced preterm birth in mice

Intra-amniotic inflammation leading to preterm birth is one of the leading causes of neonatal morbidity and mortality. We recently found that the mitochondrial levels of MNRR1 (Mitochondrial Nuclear Retrograde, Regulator 1; also called CHCHD2, AAG10, or PARK22), an important bi-organellar regulator of cellular function, are reduced in the context of inflammation and that both genetic and pharmacological increase in MNRR1 levels can counter the inflammatory profile. We show here that nitazoxanide, a clinically-approved drug, is an activator of MNRR1 and prevents preterm birth in a well-characterized murine model caused by intra-amniotic lipopolysaccharide (LPS) injection. Highlights ### Competing Interest Statement The authors have declared no competing interest.