美国得克萨斯大学西南医学中心Samir M. Parikh团队的一项最新研究发现了胎盘烟酰胺腺嘌呤二核苷酸调节分娩时间。相关论文于2026年6月11日发表在《科学》杂志上。

研究组报告胎盘烟酰胺腺嘌呤二核苷酸（NAD+）动态调节妊娠长度。小鼠胎盘NAD+的消耗引起分娩，NAD+作为15-羟基前列腺素脱氢酶的辅助因子介导，该酶负责抑制前列腺素的积累。在基线和早产模型中，增加胎盘NAD+延长妊娠。这些发现表明代谢性衰竭在诱发分娩中起着核心作用，并揭示了早产和引产优化的潜在治疗途径。

据了解，分娩是由妊娠组织内的前列腺素信号介导的，在胎儿发育正常后分娩是受到严格调节的。伴随孕龄的代谢变化被认为是生育时间的决定因素，但具体的营养物质、传感器和信使仍然不清楚。

附：英文原文

Title: Placental nicotinamide adenine dinucleotide modulates the timing of labor

Author: Erin J. Ciampa, Luana M. Machado, Kathy J. Lee, Amanda J. Clark, Kyle Q. Vu, Nawal A. Khan, Sarah Kispert, Samantha Armstrong, Yunping Li, Ginger L. Milne, Ashley Solmonson, S. Ananth Karumanchi, Samir M. Parikh

Issue&Volume: 2026-06-11

Abstract: Labor is mediated proximately by prostaglandin signaling within gestational tissues and must be tightly regulated for birth to occur after appropriate fetal development. Metabolic changes accompanying gestational aging have been postulated as a determinant of birth timing, but specific nutrients, sensors, and messengers remain obscure. We report that placental nicotinamide adenine dinucleotide (NAD+) dynamically tunes gestational length. Depletion of placental NAD+ in mice provoked labor onset, mediated by the role of NAD+ as a cofactor for 15-hydroxy prostaglandin dehydrogenase, an enzyme responsible for suppressing prostaglandin accumulation. Augmentation of placental NAD+ prolonged gestation at baseline and in a model of preterm labor. These findings suggest a central role for metabolic exhaustion in provoking labor and reveal potential therapeutic avenues for preterm labor and the optimization of labor induction.

DOI: adz1624

Source: https://www.science.org/doi/10.1126/science.adz1624

期刊信息

Science：《科学》，创刊于1880年。隶属于美国科学促进会，最新IF：63.714

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