自噬
衰老
滋养层
生物
细胞生物学
毒物
男科
胎盘
胎儿
内科学
遗传学
怀孕
医学
毒性
细胞凋亡
作者
Qing Ling,Yufeng Zhang,Wei Chang,Siting Liu,Hua-Long Zhu,Hua Wang
出处
期刊:Chemosphere
[Elsevier]
日期:2024-04-24
卷期号:358: 142138-142138
被引量:1
标识
DOI:10.1016/j.chemosphere.2024.142138
摘要
Cadmium (Cd), a well-established developmental toxicant, accumulates in the placentae and disrupts its structure and function. Population study found adverse pregnancy outcomes caused by environmental Cd exposure associated with cell senescence. However, the role of autophagy activation in Cd-induced placental cell senescence and its reciprocal mechanisms are unknown. In this study, we employed animal experiments, cell culture, and case-control study to investigate the above mentioned. We have demonstrated that exposure to Cd during gestation induces placental senescence and activates autophagy. Pharmacological and genetic interventions further exacerbated placental senescence induced by Cd through the suppression of autophagy. Conversely, activation of autophagy ameliorated Cd-induced placental senescence. Knockdown of NBR1 exacerbated senescence in human placental trophoblast cells. Further investigations revealed that NBR1 facilitated the degradation of p21 via LC3B. Our case-control study has demonstrated a positive correlation between placental senescence and autophagy activation in all-cause fetal growth restriction (FGR). These findings offer a novel perspective for mitigating placental aging and placental-origin developmental diseases induced by environmental toxicants.
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