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2021
DOI: 10.1016/j.cyto.2020.155341
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Leptin receptor stimulation in late pregnant mouse uterine tissue inhibits spontaneous contractions by increasing NO and cGMP

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Cited by 9 publications
(4 citation statements)
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“…The JAK-STAT signaling pathway sustains and stimulates the growth of primordial follicles in women, thereby regulating the oocyte growth process and consequently female fertility [44,45]. Additionally, leptin inhibits uterine contractions in mice by stimulating the JAK-STAT signaling pathway [46]. The characterization of miRNA and mRNA expression profiles in hypothalamic tissues of high-and low-follicular fertility goats reveals that the identified differential expressed genes are significantly enriched in the JAK-STAT signaling pathway [47,48].…”
Section: Discussionmentioning
confidence: 99%
“…The JAK-STAT signaling pathway sustains and stimulates the growth of primordial follicles in women, thereby regulating the oocyte growth process and consequently female fertility [44,45]. Additionally, leptin inhibits uterine contractions in mice by stimulating the JAK-STAT signaling pathway [46]. The characterization of miRNA and mRNA expression profiles in hypothalamic tissues of high-and low-follicular fertility goats reveals that the identified differential expressed genes are significantly enriched in the JAK-STAT signaling pathway [47,48].…”
Section: Discussionmentioning
confidence: 99%
“…All of these findings suggest that modulation of the arachidonic acid metabolic pathway may be a prospective therapeutic strategy to alleviate symptoms in women with RSA. It has also been reported that the adipokine leptin can inhibit spontaneous and oxytocin-induced myometrial contractions by increasing NO and cGMP through stimulation of short-type leptin receptors and activation of the NO pathway in a JAK/STAT-dependent manner [ 87 ]. However, this trial demonstrated the inhibitory effect of leptin on uterine contractions only in late pregnancy, and it is not yet known whether it can be used in early pregnancy to reduce the incidence of spontaneous miscarriage.…”
Section: Abnormal Metabolism and Miscarriagementioning
confidence: 99%
“…In addition, as described by Childs et al leptin-deficient mice are infertile, and the administration of exogenous LEP is able to restore fertility [7]. LEP exerts its actions through its receptor, LEPR, a single transmembrane protein made of 874 amino acids, expressed in the brain and peripheral tissues as kidneys, lungs, stomach, endometrium, placenta and umbilical cord [8,9]. Not only LEP alterations but also LEPR ones seem to have repercussions for reproduction and pregnancy; Pérez-Pérez et al theorized that LEP and LEPR anomalies could be implicated in the pathogenesis of recurrent miscarriage, pre-eclampsia and intrauterine growth restriction [4].…”
Section: Introductionmentioning
confidence: 97%