The Molecular Mechanisms of Term and Preterm Labor: Recent Progress and Clinical Implications

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Abstract
Human parturition is characterized by a complex interplay of autocrine/paracrine factors and signaling molecules within intrauterine tissues. The prevailing view is that factors produced locally within the placenta, fetal membranes and uterus, in concert with unidentified signals originating from the fetus, act in a complex but coordinated fashion to initiate parturition at term. The questions still remain: Is preterm labor (PTL) the result of the untimely activation of normal labor-induction processes or do pathophysiologic events disturb a sensitive equilibrium and precipitate labor through abnormal mechanisms? In the light of the current view of preterm labor as a syndrome, which is reflective of multiple causes, an answer to this question could prove invaluable in addressing the requirements of the physician for accurate diagnostic tools and effective interventions for the prevention and treatment of PTL. In this article we will discuss some of the current concepts of the biochemical and molecular mechanisms involved in determining the onset of parturition in women (both at term and preterm). We have approached this article from the perspective that the initiation of labor, (that is, the progression from a state of uterine quiescence to uterine activation) is the result of changes in myometrial sensitivity and concentrations of uterotonic agents within intrauterine tissues. This view is summarized in the diagram above (see Figure 1).

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