ArticleActa physiologica (Oxford, England)2025
Maternal Diet-Induced Excess Adiposity in Mice Disrupts Mid-Gestation Decidual Immune and Vascular Homeostasis Without Impairing Spiral Artery Remodeling.
Article in Acta physiologica (Oxford, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Maternal high-fat, high-sucrose diet-induced excess adiposity is linked to placental hypoxia and disruption of fetoplacental immune homeostasis in late gestation†.Biology of reproduction · 2025Article
- Maternal Diet-Induced Excess Adiposity in Mice Disrupts Mid-Gestation Decidual Immune and Vascular Homeostasis Without Impairing Spiral Artery Remodeling.Acta physiologica (Oxford, England) · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
aimMaternal excess adiposity (i.e., overweight/obesity) is linked to impaired uteroplacental perfusion, compromised placental development, and increased risk of adverse pregnancy outcomes. Inflammation and immune dysregulation accompanying excess adiposity may disrupt leukocyte-mediated tissue remodeling and immunoregulation, contributing to placental dysfunction. However, the impacts of excess adiposity on populations of innate lymphoid cells and macrophages orchestrating these processes, and on the decidual microenvironment, remain understudied. Here, we used a mouse model of high-fat, high-sucrose (HFHS) diet-feeding to study the impacts of excess adiposity on decidual immune dynamics during placental development.
methodsUteroplacental tissues were collected at mid-gestation (E10.5) from mice fed a control chow (CON) or HFHS diet before and during pregnancy. Multicolour flow cytometry was used to profile decidual leukocyte composition. Spiral artery remodeling was measured using (immuno)histochemistry. Multiplex immunoassays were used to compare systemic and decidual cytokine and growth factor levels. Comparative gene expression was measured in placental tissues using a NanoString nCounter array.
resultsHFHS pregnancies had elevated decidual leukocyte abundance, with increased tissue-resident and conventional-like NK cells, and MHC-II
conclusionThese findings point towards decidual vascular inflammation and dysregulated angiogenesis during early placentation in pregnancies complicated by excess adiposity. This may stem from or induce shifts in resident immune cells, contributing to later placental dysfunction.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.