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The role of leukemia inhibitory factor in pathogenesis of pre-eclampsia: molecular and cell signaling approach

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Abstract

Endothelial dysfunction is considered as the main hallmark of Preeclampsia (PE). Despite the unknown pathogenesis of PE, different possible causes have been suggested in various studies. In this review, we first studied the Leukemia inhibitory factor (LIF) role in the related pathways to the PE pathogenesis, such as inflammation, endothelial dysfunction and hypertension. LIF can increase the expression of ICAM-1 and VCAM-1 via the JAK/STAT3 pathway, thereby inducing inflammatory responses and endothelial dysfunction. It can also be involved in the vascular vasoconstriction and hypertension by reducing the nitric oxide (NO) synthesis. Identifying the link between LIF and pathways associated with PE pathogenesis could be effective to achieve an effective PE treatment in the future.

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Abbreviations

LIF:

Leukemia inhibitory factor

LIFR:

LIF receptor

gp130:

Glycoprotein 130

JAK/STAT:

Janus kinase/signal transducer and activator of transcription

SOCS3:

Suppressor Of Cytokine Signaling 3

RhoA:

Ras homolog gene family member A

eNOS:

Endothelial nitric oxide synthase phosphorylation

NO:

Nitric oxide

MMP:

Matrix metallopeptidase

ICAM-1:

Intercellular Adhesion Molecule-1

VCAM-1:

Vascular cell adhesion protein-1

ID1:

Inhibitor of DNA binding 1

VEGF:

Vascular endothelial growth factor

NF-κB:

Nuclear factor-κB

Myl9:

Myosin regulatory light chain 9

PE:

Preeclampsia

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Acknowledgements

We wish to thank all our colleagues in Yasuj University of Medical Sciences.

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PE has conceived the manuscript and revised it. MA and ME wrote the manuscript. MA and MM design table. NE conducted revise.

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Correspondence to Parvinsadat Eslamnik.

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Abdolalian, M., Ebrahimi, M., Aghamirzadeh, M. et al. The role of leukemia inhibitory factor in pathogenesis of pre-eclampsia: molecular and cell signaling approach. J Mol Histol 52, 635–642 (2021). https://doi.org/10.1007/s10735-021-09989-7

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