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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).
[1]Brosens I, Brosens JJ, Muter J, et al., 2019. Preeclampsia: the role of persistent endothelial cells in uteroplacental arteries. Am J Obstet Gynecol, 221(3):219-226.
[2]Burton GJ, Jauniaux E, Charnock-Jones DS, 2010. The influence of the intrauterine environment on human placental development. Int J Dev Biol, 54(2-3):303-311.
[3]Chaiworapongsa T, Chaemsaithong P, Yeo L, et al., 2014. Pre-eclampsia part 1: current understanding of its pathophysiology. Nat Rev Nephrol, 10(8):466-480.
[4]Chan DC, 2006. Mitochondrial fusion and fission in mammals. Annu Rev Cell Dev Biol, 22:79-99.
[5]Chandhok G, Lazarou M, Neumann B, 2018. Structure, function, and regulation of mitofusin-2 in health and disease. Biol Rev Camb Philos Soc, 93(2):933-949.
[6]Debattisti V, Pendin D, Ziviani E, et al., 2014. Reduction of endoplasmic reticulum stress attenuates the defects caused by Drosophila mitofusin depletion. J Cell Biol, 204(3):303-312.
[7]Du L, He F, Kuang L, et al., 2017. eNOS/iNOS and endoplasmic reticulum stress-induced apoptosis in the placentas of patients with preeclampsia. J Hum Hypertens, 31(1):49-55.
[8]Eddy AC, Chapman H, George EM, 2019. Acute hypoxia and chronic ischemia induce differential total changes in placental epigenetic modifications. Reprod Sci, 26(6):766-773.
[9]Genbacev O, Miller RK, 2000. Post-implantation differentiation and proliferation of cytotrophoblast cells: in vitro models—a review. Placenta, 21(Suppl A):S45-S49.
[10]Lorenzon-Ojea AR, Yung HW, Burton GJ, et al., 2020. The potential contribution of stromal cell-derived factor 2 (SDF2) in endoplasmic reticulum stress response in severe preeclampsia and labor-onset. Biochim Biophys Acta-Mol Basis Dis, 1866(2):165386.
[11]Muñoz JP, Ivanova S, Sánchez-Wandelmer J, et al., 2013. Mfn2 modulates the UPR and mitochondrial function via repression of PERK. EMBO J, 32(17):2348-2361.
[12]Ngoh GA, Papanicolaou KN, Walsh K, 2012. Loss of mitofusin 2 promotes endoplasmic reticulum stress. J Biol Chem, 287(24 ): 20321-20332.
[13]Schneeberger M, Dietrich MO, Sebastián D, et al., 2013. Mitofusin 2 in POMC neurons connects ER stress with leptin resistance and energy imbalance. Cell, 155(1):172-187.
[14]Song MS, Mihara K, Chen Y, et al., 2015. Mitochondrial fission and fusion factors reciprocally orchestrate mitophagic culling in mouse hearts and cultured fibroblasts. Cell Metab, 21(2):273-286.
[15]Steegers EAP, von Dadelszen P, Duvekot JJ, et al., 2010. Pre-eclampsia. Lancet, 376(9741):631-644.
[16]Yu J, Guo XJ, Chen RB, et al., 2016. Downregulation of mitofusin 2 in placenta is related to preeclampsia. Biomed Res Int, 2016:6323086.
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