Cell-free fetal DNA impairs trophoblast migration in a TLR9-dependent manner and can be reversed by hydroxychloroquine

Leon-Martinez, Daisy; Lynn, Tatyana; Abrahams, Vikki M.

doi:10.1016/j.jri.2023.103945

Cited by 1 publication

(1 citation statement)

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“…The exception was IL-10 secretion, where HCQ increased basal secretion by term placenta explants as well as reversed the negative effect of TLR7 agonist on term placenta explants IL-10 production ( Scott et al, 2019 ). HCQ could most likely improve migration and invasion in early placentation through a TLR9-dependent manner, as this concept was tested in trophoblast cell lines and placental explants ( He et al, 2018 ; Scott et al, 2019 ; Leon-Martinez et al, 2023 ).…”

Section: Hydroxychloroquine (Hcq)mentioning

confidence: 99%

Deciphering the immunological interactions: targeting preeclampsia with Hydroxychloroquine’s biological mechanisms

Gajić,

Schröder-Heurich,

Mayer-Pickel

2024

Front. Pharmacol.

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Preeclampsia (PE) is a complex pregnancy-related disorder characterized by hypertension, followed by organ dysfunction and uteroplacental abnormalities. It remains a major cause of maternal and neonatal morbidity and mortality worldwide. Although the pathophysiology of PE has not been fully elucidated, a two-stage model has been proposed. In this model, a poorly perfused placenta releases various factors into the maternal circulation during the first stage, including pro-inflammatory cytokines, anti-angiogenic factors, and damage-associated molecular patterns into the maternal circulation. In the second stage, these factors lead to a systemic vascular dysfunction with consecutive clinical maternal and/or fetal manifestations. Despite advances in feto-maternal management, effective prophylactic and therapeutic options for PE are still lacking. Since termination of pregnancy is the only curative therapy, regardless of gestational age, new treatment/prophylactic options are urgently needed. Hydroxychloroquine (HCQ) is mainly used to treat malaria as well as certain autoimmune conditions such as systemic lupus and rheumatoid arthritis. The exact mechanism of action of HCQ is not fully understood, but several mechanisms of action have been proposed based on its pharmacological properties. Interestingly, many of them might counteract the proposed processes involved in the development of PE. Therefore, based on a literature review, we aimed to investigate the interrelated biological processes of HCQ and PE and to identify potential molecular targets in these processes.

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