Preterm birth is defined as any delivery before 37 complete weeks of gestation. It is a universal challenge in the field of obstetrics owing to its high rate of mortality, long-term morbidity, associated human suffering and economic burden. In the United States, about 12.18% deliveries in 2009 were preterm, producing an exorbitant cost of $5.8 billion.
Infection-associated premature
rupture of membranes (PROM) accounts for 40% of extremely
preterm births (<28 weeks of gestation). Major research efforts are directed towards improving the understanding of the pathophysiology of
preterm birth and ways to prevent or at least postpone delivery.
Endothelin-1 (ET-1) is a potent
vasoconstrictor that plays a significant role in
infection-triggered
preterm birth. Its involvement in a number of pathological mechanisms and its elevation in preterm delivered amniotic fluid samples implicate it in
preterm birth.
Sphingosine kinase (SphK) is a ubiquitous
enzyme responsible for the production of
sphingosine-1-phosphate (S1P). S1P acts as second messenger in a number of cell proliferation and survival pathways. SphK is found to play a key role in ET-1 mediated myometrial contraction. This review highlights SphK as a prospective target with great potential to prevent
preterm birth.