Birth and death: Evidence for the same biologic clock
Birth and death: Evidence for the same biologic clock
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DOI：
10.1111/aji.12638
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发表时间：
2017-05-01
影响因子：
3.6
通讯作者：
Phillippe, Shiela M.
中科院分区：
文献类型：
--
作者：
Phillippe, Mark;Phillippe, Shiela M.
在哺乳动物中，平均寿命（以年为单位）和妊娠期（以天为单位）之间存在很强的相关性，这表明相同的生物钟机制控制着这两种生理事件。寿命是由一系列导致生物体衰老并最终死亡的复杂事件决定的。尽管认为涉及多种生物化学和细胞现象，但由于DNA复制期间的氧化应激和损失而导致的进行性端粒缩短被认为是促成衰老、衰老和成年死亡的重要决定因素。我们推测，类似的生化和细胞现象发生在胎盘和胎膜中，导致它们在妊娠期间老化，它们在足月时衰老，以及它们的凋亡性死亡，导致以胎儿无细胞DNA形式释放炎性介质。本文综述了支持端粒妊娠时钟假说的证据，该假说提出妊娠组织（特别是胎盘和胎膜）中的端粒进行性缩短导致细胞凋亡和胎儿游离DNA释放，从而刺激促炎信号级联反应，驱动分娩的进展。
In mammals, there exists a strong correlation between the average life span (in years) and the length of gestation (in days), suggesting that the same biologic clock mechanisms control both of these physiologic events. Life span is determined by a complex sequence of events leading to organismal senescence, and ultimately death. Although multiple biochemical and cellular phenomena are believed to be involved, progressive telomere shortening due to oxidative stress and loss during DNA replication is believed to be an important determinant contributing to aging, senescence, and adult death. We hypothesize that similar biochemical and cellular phenomena occur in the placenta and fetal membranes resulting in their aging during gestation, their senescence at term, and their apoptotic death resulting in the release of an inflammatory mediator in the form of fetal cell-free DNA. This article reviews the evidence supporting this telomere gestational clock hypothesis which proposes that progressive telomere shortening in gestational tissue (especially the placenta and fetal membranes) leads to apoptosis and fetal cell-free DNA release, thereby stimulating the proinflammatory signaling cascade that drives the progression of parturition.