Myometrial Research Laboratory, University of Nevada School of Medicine, Reno, Nevada 89557-0573, USA.
Acta Pharmacol Sin. 2011 Jun;32(6):758-64. doi: 10.1038/aps.2011.62.
Rates of premature birth are alarming and threaten societies and healthcare systems worldwide. Premature labor results in premature birth in over 50% of cases. Preterm birth accounts for three-quarters of infant morbidity and mortality. Children that survive birth before 34 weeks gestation often face life-long disability. Current treatments for preterm labor are wanting. No treatment has been found to be generally effective and none are systematically evaluated beyond 48 h. New approaches to the treatment of preterm labor are desperately needed. Recent studies from our laboratory suggest that the uterine muscle is a unique compartment with regulation of uterine relaxation unlike that of other smooth muscles. Here we discuss recent evidence that the mechanically activated 2-pore potassium channel, TREK-1, may contribute to contraction-relaxation signaling in uterine smooth muscle and that TREK-1 gene variants associated with human labor and preterm labor may lead to a better understanding of preterm labor and its possible prevention.
早产率令人震惊，威胁着全世界的社会和医疗保健系统。超过 50%的早产病例是由早产引起的。早产占婴儿发病率和死亡率的四分之三。在妊娠 34 周前出生的儿童往往面临终身残疾。目前治疗早产的方法不尽如人意。尚未发现一种治疗方法普遍有效，也没有一种方法在 48 小时后得到系统评估。迫切需要新的方法来治疗早产。我们实验室最近的研究表明，子宫肌肉是一个独特的隔室，其松弛调节不同于其他平滑肌。在这里，我们讨论了最近的证据，即机械激活的 2 孔钾通道 TREK-1 可能有助于子宫平滑肌的收缩-松弛信号转导，并且与人类分娩和早产相关的 TREK-1 基因变异可能有助于更好地理解早产及其可能的预防。
