Evidence map›Paper›PMID 36748194›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2023

FoxO1 Deficiency Enhances Cell Proliferation and Survival Under Normoglycemia and Promotes Angiogenesis Under Hyperglycemia in the Placenta.

Zehuan Ding, Naomi McCauley, Yushu Qin, Lauren Lawless, Shaodong Guo, Lanjing Zhang, Ke K Zhang, Linglin Xie

Open access · bronzeAbstract read
In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.3field-weighted citation impact, top 38% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 2 citations in OpenAlex.

  1. Review
  2. Article
  3. Frontiers in cellular and infection microbiology · 2025
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Zehuan DingDepartment of Nutrition, Texas A&M University, College Station, Texas.
Naomi McCauleyDepartment of Nutrition, Texas A&M University, College Station, Texas.
Yushu QinDepartment of Nutrition, Texas A&M University, College Station, Texas.
Lauren LawlessDepartment of Nutrition, Texas A&M University, College Station, Texas.
Shaodong GuoDepartment of Nutrition, Texas A&M University, College Station, Texas.
Lanjing ZhangDepartment of Pathology, Princeton Medical Center, Plainsboro, New Jersey; Department of Biological Sciences, Rutgers University, Newark, New Jersey.
Ke K ZhangDepartment of Nutrition, Texas A&M University, College Station, Texas; Center for Epigenetics & Disease Prevention, Institute of Biosciences & Technology, College of Medicine, Texas A&M University, Houston, Texas.
Linglin XieDepartment of Nutrition, Texas A&M University, College Station, Texas. Electronic address: Linglin.xie@agnet.tamu.edu.
Texas A&M University · USRutgers, The State University of New Jersey · USTexas A&M University System · US

Funding

Texas A&M Center for Environmental Health Research (TiCER)P30ES029067 · NIEHS · TEXAS A&M UNIVERSITY · PI Galen Newman · 2019 to 2026
$13.0M
NIEHS NIH HHS P30 ES029067
6 · The paper itself

Abstract

FoxO1 is an important transcriptional factor that regulates cell survival and metabolism in many tissues. Deleting FoxO1 results in embryonic death due to failure of chorioallantoic fusion at E8.5; however, its role in placental development during mid-late gestation is unclear. In both human patients with gestational diabetes and pregnant mice with hyperglycemia, placental FoxO1 expression was significantly increased. Using FoxO1+/- mice, the effects of FoxO1 haploinsufficiency on placental development under normoglycemia and hyperglycemia were investigated. With FoxO1 haploinsufficiency, the term placental weight increased under both normal and hyperglycemic conditions. Under normoglycemia, this weight change was associated with a general enlargement of the labyrinth, along with increased cell proliferation, decreased cell apoptosis, and decreased expression of p21, p27, Casp3, Casp8, and Rip3. However, under hyperglycemia, the placental weight change was associated with increased fetal blood space, VEGFA overexpression, and expression changes of the angiogenic markers, Eng and Tsp1. In conclusion, FoxO1 plays a role in regulating cell proliferation, cell survival, or angiogenesis, depending on blood glucose levels, during placenta development.

Indexed as

Diabetes, GestationalForkhead Box Protein O1HyperglycemiaAnimalsCell ProliferationFemaleGene Expression RegulationHumansMicePlacentaPregnancyForkhead Box Protein O1FOXO1 protein, humanFoxo1 protein, mouseangiogenesisapoptosisFoxO1hyperglycemiaplacental developmentproliferation

Identifiers

PMID36748194
PMCPMC11890199
OpenAlexW4316810260

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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 OpenQuestion graph.