NIH R01 · 2024
A novel molecular mechanism for stimulating uterine contractility by oxytocin
Project Summary During pregnancy, the uterus gradually transitions from a quiescent state characterized by weak, asynchronous, regional contractions to an activated state in which contractions increase in force, frequency, and synchrony to expel the fetus at term. A major driver of this transition is gradual depolarization of the myometrial smooth muscle cell (MSMC) membrane potential. As the inside of the membrane becomes less negatively charged, the myometrium becomes more excitable. However, the molecular pathways controlling this transition are unknown, hampering our ability to develop strategies to regulate uterine contractility to prevent pre- or post-term labor. Here, we propose to…
From the public funding record at NIH RePORTER. Describes the funded project, not the reviews below.