Evidence map›Paper›PMID 25595581›Full record

ReviewAmerican journal of obstetrics and gynecology2015

Advances in revealing the molecular targets downstream of oxidative stress-induced proapoptotic kinase signaling in diabetic embryopathy.

Fang Wang, E Albert Reece, Peixin Yang

Abstract readReview
In one paragraph

Review in American journal of obstetrics and gynecology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

36 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Dysglycemia in Pregnancy and Maternal/Fetal Outcomes.Journal of women's health (2002) · 2021
    Article
  8. Article
  9. Article
  10. Article
  11. Trehalose restores functional autophagy suppressed by high glucose.Reproductive toxicology (Elmsford, N.Y.) · 2019
    Article
  12. ASK1 induces retinal microvascular endothelial cell apoptosis through ER stress-associated pathway.International journal of clinical and experimental pathology · 2019
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Endoplasmic Reticulum Stress-Induced CHOP Inhibits PGC-1α and Causes Mitochondrial Dysfunction in Diabetic Embryopathy.Toxicological sciences : an official journal of the Society of Toxicology · 2017
    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 ReeceDepartment of Obstetrics, Gynecology, and Reproductive Sciences, University of Maryland School of Medicine, Baltimore, MD; Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, MD.
Peixin YangDepartment of Obstetrics, Gynecology, and Reproductive Sciences, University of Maryland School of Medicine, Baltimore, MD; Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, MD. Electronic address: pyang@fpi.umaryland.edu.
University of Maryland, Baltimore · US

Funding

Apoptotic Mechanism of Maternal Diabetes-Induced Neural Tube DefectsR01DK083243 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI YANG, PEIXIN · 2010 to 2019
$3.1M
Molecular Signalling Pathways and Cellular Stress in Diabetic EmbryopathyR01DK103024 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI REECE, E. ALBERT, YANG, PEIXIN · 2014 to 2017
$1.7M
Autophagy and its Regulation in Diabetic EmbryopathyR01DK101972 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI YANG, PEIXIN · 2014 to 2017
$1.6M
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 R01 DK083243NIDDK NIH HHS R01DK083243NIDDK NIH HHS R01 DK101972NIDDK NIH HHS R01DK101972NIDDK NIH HHS R01 DK103024NIDDK NIH HHS R01DK103024NIDDK NIH HHS R56 DK095380
6 · The paper itself

Abstract

Preexisting maternal diabetes is a high-risk factor of diabetic embryopathy, such as neural tube defects and congenital heart defects. Maternal diabetes significantly increases the production of reactive oxygen species, resulting in oxidative stress and diabetic embryopathy. Multiple cellular and metabolic factors contribute to these processes. Forkhead box O (FoxO)-3a has been demonstrated as a key transcription factor in the signaling transduction pathways responsible for maternal diabetes-induced birth defects. Apoptosis signal-regulating kinase 1 (ASK1) activated by oxidative stress stimulates nuclear translocation of FoxO3a, resulting in the overexpression of tumor necrosis factor receptor 1-associated death domain protein, which, in turn, leads to caspase-8 activation and apoptosis. Maternal diabetes-activated c-Jun N-terminal kinase (JNK)-1/2, downstream effectors of ASK1, can be blocked by superoxide dismutase-1 overexpression, suggesting that oxidative stress is responsible for JNK1/2 signaling activation. Deletion of JNK1/2 significantly suppressed the activity of FoxO3a. These observations indicate that maternal diabetes-induced oxidative stress stimulates the activation of ASK1, JNK1/2, FoxO3a, tumor necrosis factor receptor 1-associated death domain protein, caspase-8 cleavage, and finally, apoptosis and diabetic embryopathy.

Indexed as

ApoptosisOxidative StressCaspase 8FemaleFetal DiseasesForkhead Box Protein O3Forkhead Transcription FactorsHumansMAP Kinase Kinase Kinase 5Mitogen-Activated Protein Kinase 8Mitogen-Activated Protein Kinase 9PregnancyPregnancy in DiabeticsReceptors, Tumor Necrosis Factor, Type ISignal TransductionSuperoxide DismutaseCaspase 8Forkhead Box Protein O3Forkhead Transcription FactorsFOXO3 protein, humanMAP Kinase Kinase Kinase 5Mitogen-Activated Protein Kinase 8Mitogen-Activated Protein Kinase 9Receptors, Tumor Necrosis Factor, Type ISuperoxide Dismutaseapoptosisbirth defectskinase signalingmaternal diabetesoxidative stress

Identifiers

PMID25595581
PMCPMC4500754
OpenAlexW1968100018

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.