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Updated: May 10, 2026
A Pipeline to Investigate the Structures and Signaling Pathways of Sphingosine 1-Phosphate Receptors
Published on: June 8, 2022
Sphingosine kinase: a novel putative target for the prevention of infection-triggered preterm birth
Vibhuti Vyas1, Charles R Ashby, Sandra E Reznik
1Department of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, St. John's University, Queens, NY 11439, USA.
Insights
Preterm birth, a major obstetric concern, is linked to infection and Endothelin-1. Sphingosine kinase shows promise as a therapeutic target to prevent premature delivery.
Area of Science:
- Obstetrics and Gynecology
- Reproductive Biology
- Biochemistry
Background:
- Preterm birth presents a significant global health challenge, leading to high mortality, morbidity, and economic costs.
- Infection-associated premature rupture of membranes (PROM) is a major contributor to extremely preterm births.
- Endothelin-1 (ET-1), a potent vasoconstrictor, is implicated in infection-triggered preterm birth.
Purpose of the Study:
- To review the role of Endothelin-1 (ET-1) in preterm birth.
- To explore the involvement of Sphingosine kinase (SphK) in ET-1 mediated pathways.
- To identify SphK as a potential therapeutic target for preventing preterm birth.
Main Methods:
- Literature review focusing on the pathophysiology of preterm birth.
- Analysis of the role of ET-1 and SphK in myometrial contraction.
- Examination of S1P signaling pathways.
Main Results:
- ET-1 is significantly elevated in preterm birth cases and contributes to myometrial contraction.
- SphK plays a crucial role in ET-1 mediated myometrial contraction.
- SphK is involved in cell proliferation and survival pathways through S1P production.
Conclusions:
- SphK is a key mediator in the pathway leading to infection-associated preterm birth.
- Targeting SphK offers a promising strategy for the prevention of preterm birth.
- Further research into SphK inhibitors could lead to novel therapeutic interventions.
Abstract:
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.
