
doi: 10.1530/rep.1.00197
pmid: 16264088
Abstract Preterm birth remains the leading cause of perinatal mortality and morbidity, largely as a result of a poor understanding of the precise mechanisms controlling labour onset in humans. Inflammation has long been recognised as a key feature of both preterm and term labour, with an influx of inflammatory cells into the uterus and elevated levels of pro-inflammatory cytokines observed during parturition. Nuclear factor kappa B (NF-κB) is a transcription factor family classically associated with inflammation. Accumulating evidence points to a role for NF-κB in the physiology and pathophysiology of labour. NF-κB activity increases with labour onset and is central to multiple prolabour pathways. Premature or aberrant activation of NF-κB may thus contribute to preterm labour. The current understanding of NF-κB in the context of human labour is discussed here.
Inflammation, NF-kappa B, Matrix Metalloproteinases, Mice, Obstetric Labor, Premature, Pregnancy, Prostaglandins, Animals, Cytokines, Humans, Labor Onset, Female, I-kappa B Proteins, Signal Transduction
Inflammation, NF-kappa B, Matrix Metalloproteinases, Mice, Obstetric Labor, Premature, Pregnancy, Prostaglandins, Animals, Cytokines, Humans, Labor Onset, Female, I-kappa B Proteins, Signal Transduction
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