Evidence map›Paper›PMID 37497595›Full record

ReviewBirth defects research2023

Epigenetic implications in maternal diabetes and metabolic syndrome-associated risk of orofacial clefts.

Bo Sun, Kurt S Reynolds, Michael A Garland, Moira McMahon, Subbroto K Saha, Chengji J Zhou

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Birth defects research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 11% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. The Role ofJournal of clinical medicine · 2024
    Review
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

6 authors at 1 institution in 1 country.

Bo SunDepartment of Biochemistry and Molecular Medicine, University of California at Davis, School of Medicine, Sacramento, California, USA.
Kurt S ReynoldsDepartment of Biochemistry and Molecular Medicine, University of California at Davis, School of Medicine, Sacramento, California, USA.
Michael A GarlandDepartment of Biochemistry and Molecular Medicine, University of California at Davis, School of Medicine, Sacramento, California, USA.
Moira McMahonDepartment of Biochemistry and Molecular Medicine, University of California at Davis, School of Medicine, Sacramento, California, USA.
Subbroto K SahaDepartment of Biochemistry and Molecular Medicine, University of California at Davis, School of Medicine, Sacramento, California, USA.
Chengji J ZhouDepartment of Biochemistry and Molecular Medicine, University of California at Davis, School of Medicine, Sacramento, California, USA.ORCID 0000-0001-8592-4680
Shriners Hospitals for Children - Erie · US

Funding

Cellular and molecular mechanisms of orofacial cleftsR01DE026737 · NIDCR · UNIVERSITY OF CALIFORNIA AT DAVIS · PI ZHOU, CHENGJI · 2017 to 2021
$3.1M
Surface ectodermal mechanism and maternal intervention of neural tube defectsR01NS102261 · NINDS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI ZHOU, CHENGJI · 2018 to 2022
$2.5M
NIDCR NIH HHS R01 DE026737NIH HHS R01DE026737NIH HHS R01NS102261NINDS NIH HHS R01 NS102261
6 · The paper itself

Abstract

Orofacial clefts (OFCs) are one of the most common types of structural birth defects. The etiologies are complicated, involving with genetic, epigenetic, and environmental factors. Studies have found that maternal diabetes and metabolic syndrome are associated with a higher risk of OFCs in offspring. Metabolic syndrome is a clustering of several disease risk factors, including hyperglycemia, dyslipidemia, obesity, and hypertension. Metabolic disease during pregnancy can increase risk of adverse outcomes and significantly influence fetal development, including orofacial formation and fusion. An altered metabolic state may contribute to developmental disorders or congenital defects including OFCs, potentially through epigenetic modulations, such as histone modification, DNA methylation, and noncoding RNA expression to alter activities of critical morphogenetic signaling or related developmental genes. This review summarizes the currently available evidence and underlying mechanisms of how the maternal metabolic syndrome is associated with OFCs in mostly human and some animal studies. It may provide a better understanding of the interactions between intrauterine metabolic status and fetal orofacial development which might be applied toward prevention and treatments of OFCs.

Indexed as

Cleft LipCleft PalateDiabetes, GestationalMetabolic SyndromeAnimalsEpigenesis, GeneticFemaleHumansPregnancydiabetesdyslipidemiaepigeneticshypertensionmaternal metabolic syndromeobesityorofacial clefts

Identifiers

PMID37497595
PMCPMC11526419
OpenAlexW4385294640

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.