Uterine ion channels offer potential new target to delay preterm birth
Scientists have found that targeting a particular group of proteins in the uterus muscle (myometrium) can suppress human uterine contractions in laboratory studies and delay preterm birth in a preclinical model.
Scientists have discovered that targeting specific proteins in the uterus muscle (myometrium) may offer a new approach to delaying preterm birth. The study, published in Communications Medicine, suggests that inhibiting a group of proteins called KV7 channels could potentially reduce uterine contractions and delay preterm birth.
Preterm birth, defined as birth before 37 weeks of pregnancy, affects around 1 in 12 babies in the UK and poses significant risks for neonatal health. Currently, limited treatment options exist for preventing spontaneous preterm birth, as the biological pathways that trigger labor are not fully understood. Professor Rachel Tribe from King's College London emphasized the importance of developing new treatments to improve outcomes for babies born too soon.
The research team identified KV7 channels present in the myometrium of both term and preterm pregnancies, indicating their potential as drug targets. The activation of these channels, using a drug called retigabine, was found to reduce uterine contractions in both human tissue and mouse models. The findings provide a proof-of-principle for the development of new drugs or repurposing existing ones that specifically target KV7 channels in the uterus.
Further research is needed to evaluate the benefits to neonates and to explore innovative drug-delivery systems that target the uterus.
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