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

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.

Automated summary

Endothelial dysfunction is considered the main characteristic of Preeclampsia, with possible causes including inflammation, endothelial dysfunction, and hypertension. LIF can induce inflammatory responses and endothelial dysfunction via the JAK/STAT3 pathway, as well as contribute to vasoconstriction and hypertension by reducing nitric oxide synthesis. Identifying the link between LIF and pathways related to Preeclampsia pathogenesis may lead to effective treatments in the future.