Polettini J, Dutta E H, Behnia F, Saade G R, Torloni M R, Menon R
Division of Maternal-Fetal Medicine and Perinatal Research, Department of Obstetrics and Gynecology, The University of Texas Medical Branch at Galveston, Galveston, TX, USA; Department of Pathology, Botucatu Medical School, UNESP - Univ. Estadual Paulista, Botucatu, São Paulo, Brazil.
Division of Maternal-Fetal Medicine and Perinatal Research, Department of Obstetrics and Gynecology, The University of Texas Medical Branch at Galveston, Galveston, TX, USA.
Placenta. 2015 Sep;36(9):969-73. doi: 10.1016/j.placenta.2015.05.003. Epub 2015 May 9.
Many adverse pregnancy outcomes (APOs), including spontaneous preterm birth (PTB), are associated with placental dysfunction. Recent clinical and experimental evidences suggest that premature aging of the placenta may be involved in these events. Although placental aging is a well-known concept, the mechanisms of aging during normal pregnancy and premature aging in APOs are still unclear. This review was conducted to assess the knowledge on placental aging related biochemical changes leading to placental dysfunction in PTB and/or preterm premature rupture of membranes (pPROM).
We performed a systematic review of studies published over the last 50 years in two electronic databases (Pubmed and Embase) on placental aging and PTB or pPROM.
The search yielded 554 citations, 30 relevant studies were selected for full-text review and three were included in the review. Only one study reported oxidative stress-related aging and degenerative changes in human placental membranes and telomere length reduction in fetal cells as part of PTB and/or pPROM mechanisms. Similarly, two animal studies reported findings of decidual senescence and referred to PTB mechanisms.
Placental and fetal membrane oxidative damage and telomere reduction are linked to premature aging in PTB and pPROM but the risk factors and biomolecular pathways causing this phenomenon are not established in the literature. However, no biomarkers or clinical indicators of premature aging as a pathology of PTB and pPROM have been reported. We document major knowledge gaps and propose several areas for future research to improve our understanding of premature aging linked to placental dysfunction.
许多不良妊娠结局(APO),包括自发性早产(PTB),都与胎盘功能障碍有关。最近的临床和实验证据表明,胎盘过早老化可能与这些事件有关。虽然胎盘老化是一个众所周知的概念,但正常妊娠期间的老化机制以及APO中的过早老化机制仍不清楚。本综述旨在评估与胎盘老化相关的生化变化的知识,这些变化会导致PTB和/或胎膜早破(pPROM)中的胎盘功能障碍。
我们对过去50年在两个电子数据库(PubMed和Embase)中发表的关于胎盘老化与PTB或pPROM的研究进行了系统综述。
检索得到554条引文,选择30项相关研究进行全文审查,其中3项纳入综述。只有一项研究报告了人胎盘膜中与氧化应激相关的老化和退行性变化以及胎儿细胞端粒长度缩短,作为PTB和/或pPROM机制的一部分。同样,两项动物研究报告了蜕膜衰老的结果并提及了PTB机制。
胎盘和胎膜的氧化损伤以及端粒缩短与PTB和pPROM中的过早老化有关,但导致这种现象的风险因素和生物分子途径在文献中尚未明确。然而,尚未有作为PTB和pPROM病理学的过早老化的生物标志物或临床指标的报道。我们记录了主要的知识空白,并提出了几个未来研究领域,以增进我们对与胎盘功能障碍相关的过早老化的理解。