Maternal obesity: new placental paradigms unfolded

被引:21
|
作者
Brombach, Carolin [1 ]
Tong, Wen [2 ,3 ,4 ]
Giussani, Dino A. [2 ,3 ,4 ,5 ]
机构
[1] Karolinska Inst, S-17177 Stockholm, Sweden
[2] Univ Cambridge, Dept Physiol Dev & Neurosci, Cambridge CB2 3EL, England
[3] Univ Cambridge, Ctr Trophoblast Res, Cambridge CB2 3EG, England
[4] Cambridge Strateg Res Initiat Reprod, Cambridge CB2 3EL, England
[5] Cambridge Cardiovasc Ctr Res Excellence, Cambridge CB2 0QQ, England
基金
英国医学研究理事会;
关键词
ENDOPLASMIC-RETICULUM STRESS; GESTATIONAL DIABETES-MELLITUS; HIGH-FAT DIET; UMBILICAL BLOOD-FLOW; OXIDATIVE STRESS; PROTEIN RESPONSE; MITOCHONDRIAL-FUNCTION; SUBSTRATE REQUIREMENTS; GLUCOSE-METABOLISM; FETAL OVERGROWTH;
D O I
10.1016/j.molmed.2022.05.013
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The prevalence of maternal obesity is increasing at an alarming rate, and is provid-ing a major challenge for obstetric practice. Adverse effects on maternal and fetal health are mediated by complex interactions between metabolic, inflammatory, and oxidative stress signaling in the placenta. Endoplasmic reticulum (ER) stress and activation of the unfolded protein response (UPR) are common downstream pathways of cell stress, and there is evidence that this conserved homeostatic response may be a key mediator in the pathogenesis of placental dysfunction. We summarize the current literature on the placental cellular and molecular changes that occur in obese women. A special focus is cast onto placental ER stress in obese pregnancy, which may provide a novel link for future investigation.
引用
收藏
页码:823 / 835
页数:13
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