Leptin Dynamics in Pregnancy and Preeclampsia
Summary
Leptin, a peptide hormone traditionally associated with energy homeostasis, acquires additional roles in pregnancy through placental secretion. Circulating leptin concentrations rise steadily during the first and second trimesters, peaking around mid-gestation before declining postpartum. In normal gestation leptin supports trophoblast proliferation, invasion and angiogenesis, and modulates maternal immune tolerance. In preeclampsia, characterised by new-onset hypertension and end-organ dysfunction after 20 weeks’ gestation, leptin is dysregulated at maternal, placental and fetal interfaces. Hyperleptinaemia contributes to endothelial activation, exacerbates a pro-inflammatory milieu and may impair cytotrophoblast invasion through aberrant receptor signalling. Interactions between leptin and anti-angiogenic factors such as soluble fms-like tyrosine kinase-1 (sFlt-1) and reduced placental growth factor (PlGF), together with activation of STAT, NF-κB and MAPK cascades, underpin a feed-forward loop that amplifies placental dysfunction, hypertension and fetal growth restriction. Enhanced understanding of leptin’s mechanistic contributions has highlighted its potential as an early biomarker and as a target for interventions aimed at restoring placental homeostasis.
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Leptin Dynamics in Pregnancy and Preeclampsia publication trend
The graph below shows the total number of articles in leptin dynamics in pregnancy and preeclampsia across all publications each year (not limited to Nature Index journals).
Technical terms
Leptin: Peptide hormone produced by adipocytes and placenta that regulates energy balance, trophoblast function and immune responses.
Preeclampsia: Pregnancy-specific hypertensive disorder with multi-organ involvement arising after 20 weeks’ gestation.
Hofbauer cells: Fetal-origin macrophages in placental villi that mediate local immune and inflammatory processes.
Cytotrophoblast: Proliferative placental cell lineage that invades the maternal decidua to establish uteroplacental circulation.
ERK1/2 MAPK pathway: Intracellular kinase cascade transmitting signals from hormones and growth factors to regulate gene expression.
sFlt-1: Soluble fms-like tyrosine kinase-1, an anti-angiogenic factor elevated in preeclampsia that binds and neutralises pro-angiogenic ligands.
PlGF: Placental growth factor, a pro-angiogenic cytokine essential for vascular development, typically reduced in preeclampsia.
References
- Leptin-Mediated Induction of IL-6 Expression in Hofbauer Cells Contributes to Preeclampsia Pathogenesis. International Journal of Molecular Sciences (2023).
- The effects of leptin on human cytotrophoblast invasion are gestational age and dose-dependent. Frontiers in Endocrinology (2024).
- Leptin action in normal and pathological pregnancies. Journal of Cellular and Molecular Medicine (2017).
- Changes in pregnancy-related serum biomarkers early in gestation are associated with later development of preeclampsia. PLOS ONE (2020).
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