Evidence map›Paper›PMID 23791840›Full record

ArticleAmerican journal of obstetrics and gynecology2013

Superoxide dismutase 1 overexpression in mice abolishes maternal diabetes-induced endoplasmic reticulum stress in diabetic embryopathy.

Fang Wang, E Albert Reece, Peixin Yang

Open access · greenAbstract read
In one paragraph

Article in American journal of obstetrics and gynecology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
6.6field-weighted citation impact, top 3% 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

47 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
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  14. Environmental Risk Factors for Congenital Heart Disease.Cold Spring Harbor perspectives in biology · 2020
    Review
  15. Review
  16. Article
  17. Article
  18. Trehalose restores functional autophagy suppressed by high glucose.Reproductive toxicology (Elmsford, N.Y.) · 2019
    Article
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

Fang WangDepartment of Obstetrics, Gynecology, and Reproductive Sciences, University of Maryland School of Medicine, Baltimore, MD.
E Albert Reece
Peixin Yang
University of Maryland, Baltimore · US

Funding

JHU-UMD Diabetes Research CenterP30DK079637 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI AHIMA, REXFORD S. · 2013 to 2017
$9.7M
Apoptotic Mechanism of Maternal Diabetes-Induced Neural Tube DefectsR01DK083243 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI YANG, PEIXIN · 2010 to 2019
$3.1M
Autophagy and its Regulation in Diabetic EmbryopathyR01DK101972 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI YANG, PEIXIN · 2014 to 2017
$1.6M
Mechanisms of Diabetic Embryopathy and Molecular PathwaysR01DK083770 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI REECE, E. ALBERT · 2008 to 2011
$1.3M
Metabolic Cellular Stress and its Regulatory Mechanism in Diabetic EmbryopathyR56DK095380 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI YANG, PEIXIN · 2012 to 2012
$150k
NIDDK NIH HHS P30 DK079637NIDDK NIH HHS R01 DK083243NIDDK NIH HHS R01DK083243NIDDK NIH HHS R01 DK083770NIDDK NIH HHS R01 DK101972NIDDK NIH HHS R56 DK095380
6 · The paper itself

Abstract

objectiveBoth oxidative stress and endoplasmic reticulum stress (ER stress) are causal events in diabetic embryopathy. We tested whether oxidative stress causes ER stress. STUDY

designWild-type (WT) and superoxide dismutase 1 (SOD1)-overexpressing day 8.75 embryos from nondiabetic WT control with SOD1 transgenic male and diabetic WT female with SOD1 transgenic male were analyzed for ER stress markers: C/EBP-homologous protein (CHOP), calnexin, eukaryotic initiation factor 2α (eIF2α), protein kinase ribonucleic acid (RNA)-like ER kinase (PERK), binding immunoglobulin protein, protein disulfide isomerase family A member 3, kinases inositol-requiring protein-1α (IRE1α), and the X-box binding protein (XBP1) messenger RNA (mRNA) splicing.

resultsMaternal diabetes significantly increased the levels of CHOP, calnexin, phosphorylated (p)-eIF2α, p-PERK, and p-IRE1α; triggered XBP1 mRNA splicing; and enhanced ER chaperone gene expression in WT embryos. SOD1 overexpression blocked these diabetes-induced ER stress markers.

conclusionMitigating oxidative stress via SOD1 overexpression blocks maternal diabetes-induced ER stress in vivo.

Indexed as

AnimalsCalnexinDisease Models, AnimalDNA-Binding ProteinseIF-2 KinaseEmbryo, MammalianEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressEndoribonucleasesEukaryotic Initiation Factor-2FemaleFetal DiseasesHeat-Shock ProteinsMaleMiceMice, Inbred C57BLCalnexinDdit3 protein, mouseDNA-Binding ProteinseIF-2 KinaseEndoplasmic Reticulum Chaperone BiPEndoribonucleasesErn1 protein, mouseEukaryotic Initiation Factor-2Heat-Shock ProteinsPdia3 protein, mouseProtein Disulfide-IsomerasesProtein Serine-Threonine KinasesRegulatory Factor X Transcription FactorsSod1 protein, mouseSuperoxide DismutaseSuperoxide Dismutase-1Transcription Factor CHOPTranscription FactorsX-Box Binding Protein 1Xbp1 protein, mousediabetic embryopathyendoplasmic reticulum stressoxidative stresssuperoxide dismutase 1 transgenic mice

Identifiers

PMID23791840
PMCPMC3786037
OpenAlexW2007065615

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.