In pregnancy, it’s best for women to carry babies to full term, considered to be between 39 and 40 weeks of pregnancy. Babies born before that time run the risk of having a small birth weight. Small birth weight is associated with incomplete development and increases the risk of cardiovascular disease in children, as well as other complications later in life.
Roughly 1 in 9 births in the U.S. are preterm. Preterm, or “premature,” labor and birth are more common in pregnant women with certain risk factors including obesity, gestational diabetes and high blood pressure in pregnancy. Unfortunately, due to rising rates of these risk factors among women, preterm labor remains a serious risk in many pregnancies. Current treatment strategies for women at risk for preterm birth or who are experiencing preterm labor revolve around delaying birth to allow the fetus to continue to develop as much as possible before delivery. This includes the use of steroids to help develop the infant’s lungs (one of the last organs to mature before the baby is born) and hormones such as progesterone to prevent uterine contractions. However, what causes preterm labor to start is not fully understood.
A recent study published in The Journal of Clinical Investigation found a new protein that plays a role in starting labor in mice. In previous research, scientists linked a deficiency in surfactant protein-A (SP-A)—a protein that helps the lungs develop and is increased right before birth—to a delay in birth. The research team wanted to determine if production of this protein, and ultimately the start of labor, could be delayed by targeting the building block steroid proteins involved in SP-A development. They found that reducing the steroid precursors led to reduced levels of SP-A and longer pregnancies and also led to reductions in inflammation and other factors linked to early labor. The authors concluded that fetal lungs may send signals that help labor to start and that steroids involved in SP-A production are an important part of this process.
While this research is still in its very young stages, this study lays the groundwork that this pathway may be a potential target for medicines that prevent premature birth in high-risk pregnant women and ultimately improve fetal outcomes.
Jessica Faulkner is a graduate student in the department of pharmacology and the Cardiovascular-Renal Research Center at the University of Mississippi Medical Center.