Gargett C E, Schwab K E, Brosens J J, Puttemans P, Benagiano G, Brosens I
The Ritchie Centre, MIMR-PHI Institute of Medical Research, Clayton 3168, Australia Department of Obstetrics and Gynecology, Monash University, Clayton 3168, Australia
The Ritchie Centre, MIMR-PHI Institute of Medical Research, Clayton 3168, Australia.
Mol Hum Reprod. 2014 Jul;20(7):591-8. doi: 10.1093/molehr/gau025. Epub 2014 Mar 27.
The pathogenesis of early-onset endometriosis has recently been revisited, sparked by the discovery of endometrial stem/progenitor cells and their possible role in endometriosis, and because maternal pregnancy hormone withdrawal following delivery induces uterine bleeding in the neonate. The neonatal uterus has a large cervix to corpus ratio which is functionally blocked with mucous, supporting the concept of retrograde shedding of neonatal endometrium. Only 5% show overt bleeding. Furthermore, the presence of endometriosis in pre-menarcheal girls and even in severe stage in adolescents supports the theory that early-onset endometriosis may originate from retrograde uterine bleeding soon after birth. Endometrial stem/progenitor cells have been identified in menstrual blood suggesting that they may also be shed during neonatal uterine bleeding. Thus, we hypothesized that stem/progenitor cells present in shedding endometrium may have a role in the pathogenesis of early-onset endometriosis through retrograde neonatal uterine bleeding. During the neonatal and pre-pubertal period, shed endometrial stem/progenitor cells are postulated to survive in the pelvic cavity in the absence of circulating estrogens supported by niche cells also shed during neonatal uterine bleeding. According to this hypothesis, during thelarche, under the influence of rising estrogen levels, endometrial stem/progenitor cells proliferate and establish ectopic endometrial lesions characteristic of endometriosis. This New Research Horizon review builds on recent discussions on the pathogenesis of early-onset endometriosis and raises new avenues for research into this costly condition.
近年来，早发性子宫内膜异位症的发病机制再次受到关注，这是由子宫内膜干/祖细胞的发现及其在子宫内膜异位症中可能发挥的作用引发的，同时也因为分娩后母体妊娠激素撤退会导致新生儿子宫出血。新生儿子宫的宫颈与宫体比例较大，且被黏液功能性阻塞，这支持了新生儿子宫内膜逆行脱落的概念。只有5%的新生儿出现明显出血。此外，青春期前女孩甚至青少年严重阶段存在子宫内膜异位症，这支持了早发性子宫内膜异位症可能起源于出生后不久的逆行性子宫出血这一理论。月经血中已鉴定出子宫内膜干/祖细胞，这表明它们也可能在新生儿子宫出血时脱落。因此，我们推测，脱落的子宫内膜中存在的干/祖细胞可能通过新生儿子宫逆行出血在早发性子宫内膜异位症的发病机制中发挥作用。在新生儿期和青春期前，推测脱落的子宫内膜干/祖细胞在缺乏循环雌激素的情况下，在盆腔中存活，而新生儿子宫出血时脱落的龛细胞也为其提供支持。根据这一假设，在乳房发育阶段，在雌激素水平上升的影响下，子宫内膜干/祖细胞增殖并形成子宫内膜异位症特有的异位子宫内膜病变。这篇新研究前沿综述基于最近关于早发性子宫内膜异位症发病机制的讨论，为研究这种代价高昂的疾病开辟了新的研究途径。
