ArticlePlacenta2024
Mid-late gestation leptin infusion induces placental mitochondrial and endoplasmic reticulum unfolded protein responses in a mouse model of preeclampsia.
Article in Placenta, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed.
- Vascular Endothelial Growth Factor Receptors 1 and 3 Mediate Placental Trophoblast Leptin Production in Preeclampsia, Inducing Vascular Dysfunction.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Experimental Animal Models of Preeclampsia: Mechanisms, Strengths, and Translational Relevance.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Spatially resolved fetal and maternal cell contributions to severe preeclampsia across gestation.Science advances · 2026Article
- Late-gestation mineralocorticoid receptor antagonism lowers maternal blood pressure and attenuates placental insufficiency induced by leptin in pregnant mice.American journal of physiology. Heart and circulatory physiology · 2026Article
- Article
- Navigating Cellular Stress: Endoplasmic Reticulum Stress and the Unfolded Protein Response in the Molecular Pathogenesis of Preeclampsia.Cell biochemistry and biophysics · 2025Review
- Emerging Role of Leptin in Vascular and Placental Dysfunction in Preeclampsia.Arteriosclerosis, thrombosis, and vascular biology · 2025Review
- Identification of metabolism-related subtypes and feature genes of pre-eclampsia.Scientific reports · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
introductionPreeclamptic patients, both lean and obese, present with elevated leptin levels which are associated with the development of maternal endothelial dysfunction and adverse fetal outcomes, such as growth restriction, leading to low birth weight. Recent studies in pregnant mice demonstrate that mid-late gestation leptin infusion induces clinical characteristics of preeclampsia, including elevated maternal blood pressure, maternal endothelial dysfunction and fetal growth restriction. However, whether leptin triggers placental stress responses that contribute to adverse fetal outcomes as in preeclampsia is unknown.
methodsIn the current study we measured the expression of proteins involved in the endoplasmic reticulum (UPR
resultsThe data show that mid-late gestation leptin infusion induced activation of indices of placental UPR DISCUSSION: Collectively, these data indicate that elevated levels of leptin in mid-late pregnancy in mice promote placental stress responses, akin to those in pregnant women with preeclampsia.
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