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On-line Access: 2024-08-27
Received: 2023-10-17
Revision Accepted: 2024-05-08
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Dandan SUN, Hui ZHU, Ling AI, Hanbing WU, Yanting WU, Jihua JIN. Mitochondrial fusion protein 2 regulates endoplasmic reticulum stress in preeclampsia[J]. Journal of Zhejiang University Science B, 2021, 22(2): 165-170.
@article{title="Mitochondrial fusion protein 2 regulates endoplasmic reticulum stress in preeclampsia",
author="Dandan SUN, Hui ZHU, Ling AI, Hanbing WU, Yanting WU, Jihua JIN",
journal="Journal of Zhejiang University Science B",
volume="22",
number="2",
pages="165-170",
year="2021",
publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.B2000557"
}
%0 Journal Article
%T Mitochondrial fusion protein 2 regulates endoplasmic reticulum stress in preeclampsia
%A Dandan SUN
%A Hui ZHU
%A Ling AI
%A Hanbing WU
%A Yanting WU
%A Jihua JIN
%J Journal of Zhejiang University SCIENCE B
%V 22
%N 2
%P 165-170
%@ 1673-1581
%D 2021
%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.B2000557
TY - JOUR
T1 - Mitochondrial fusion protein 2 regulates endoplasmic reticulum stress in preeclampsia
A1 - Dandan SUN
A1 - Hui ZHU
A1 - Ling AI
A1 - Hanbing WU
A1 - Yanting WU
A1 - Jihua JIN
J0 - Journal of Zhejiang University Science B
VL - 22
IS - 2
SP - 165
EP - 170
%@ 1673-1581
Y1 - 2021
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.B2000557
Abstract: Preeclampsia (PE) refers to a group of dysfunction syndromes associated with elevated blood pressure and proteinuria in women with previously normal blood pressure after 20 weeks of pregnancy, and it may be accompanied by symptoms including headache, vertigo, nausea and vomiting, and epigastric discomfort (Steegers et al., 2010). It is affected by a variety of risk factors and follows a distinctive disease progression, although its pathogenesis is still unknown. Upon termination of a PE pregnancy, the clinical symptoms of PE improve rapidly, suggesting that PE is a disease originating in the placenta. Recent studies have shown that excessive apoptosis of trophoblast cells and reduced trophoblast infiltration capacity can lead to superficial implantation of the placenta, a lack of spiral arteriole remodeling, and insufficient placental perfusion leading to placental ischemia and hypoxia, all of which are important factors that cause the onset of PE (Eddy et al., 2019). Therefore, there appears to be a close relationship between excessive trophoblast cell apoptosis and development of PE. Recently, increasing evidence has shown that in patients with PE, endoplasmic reticulum (ER) stress can cause trophoblast cell apoptosis, and this finding has become an important feature of the placental pathology of PE (Lorenzon-Ojea et al., 2020).
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