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肥胖母亲子宫瘦素信号改变:从蜕膜化受损到妊娠并发症

Altered uterine leptin signalling in obese mothers: from impaired decidualisation to pregnancy complications.

作者信息

Walewska Edyta, Hamada Zahra, Pérez-García Vicente, Galvão António

出版信息

Reproduction. 2025 Jan 9;169(2). doi: 10.1530/REP-24-0319. Print 2025 Feb 1.

DOI:10.1530/REP-24-0319
PMID:39652640
Abstract

IN BRIEF

Maternal obesity impairs uterine function, compromising embryo implantation and pregnancy establishment, posing also long-term risks to offspring health. We explore the contribution of impaired decidualisation to failed embryo implantation and placentation in obese mothers, highlighting the role of altered uterine leptin signalling in the dysregulation of extracellular matrix remodelling, vascularisation and cell proliferation and differentiation.

ABSTRACT

Obesity drastically affects maternal health and reproductive outcomes, being often associated with endocrine imbalance, compromised ovarian function and pregnancy complications. The plastic nature of pregnancy may render the developing foetus particularly vulnerable to oscillations in maternal metabolism, ultimately shaping the health trajectories of the offspring. Presently, we discuss the effect of maternal obesity on decidualisation, a critical step for embryo implantation and placental development. Decidualisation encompasses the differentiation of endometrial stromal cells into specialised decidua. Impaired decidualisation was linked to pregnancy complications, and recent studies suggest that maternal obesity has a detrimental effect on decidualisation. Leptin, an adipokine significantly increased in the circulation of obese women, is known to regulate endometrial function and decidualisation, modulating immune response, angiogenesis and cell proliferation. Furthermore, hyperleptinaemia in obese mothers was linked to altered leptin signalling in the uterus and compromised endometrial function. In this review, we explore the underlying molecular mechanisms linking altered uterine leptin signalling to impaired decidualisation and early pregnancy complications in obese mothers.

摘要

简而言之

母体肥胖会损害子宫功能,影响胚胎着床和妊娠建立,还会对后代健康构成长期风险。我们探讨了蜕膜化受损对肥胖母亲胚胎着床失败和胎盘形成的影响,强调了子宫瘦素信号改变在细胞外基质重塑、血管生成以及细胞增殖和分化失调中的作用。

摘要

肥胖严重影响母体健康和生殖结局,常与内分泌失衡、卵巢功能受损及妊娠并发症相关。妊娠的可塑性可能使发育中的胎儿特别容易受到母体代谢波动的影响,最终塑造后代的健康轨迹。目前,我们讨论母体肥胖对蜕膜化的影响,蜕膜化是胚胎着床和胎盘发育的关键步骤。蜕膜化包括子宫内膜基质细胞分化为特殊的蜕膜。蜕膜化受损与妊娠并发症有关,最近的研究表明母体肥胖对蜕膜化有不利影响。瘦素是一种在肥胖女性循环中显著增加的脂肪因子,已知其可调节子宫内膜功能和蜕膜化,调节免疫反应、血管生成和细胞增殖。此外,肥胖母亲的高瘦素血症与子宫瘦素信号改变和子宫内膜功能受损有关。在本综述中,我们探讨了将子宫瘦素信号改变与肥胖母亲蜕膜化受损和早期妊娠并发症联系起来的潜在分子机制。

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