Evidence map›Paper›PMID 33184417›Full record

ArticleScientific reports2020

Molecular pathophysiology of diabetes mellitus during pregnancy with antenatal complications.

Arthur T Kopylov, Olga Papysheva, Iveta Gribova, Galina Kotaysch, Lubov Kharitonova, Tatiana Mayatskaya, Ekaterina Sokerina, Anna L Kaysheva, Sergey G Morozov

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 2 pooled it
1.4field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 2 syntheses or guidelines pooled it, 27 citations in OpenAlex.

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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

9 authors at 4 institutions in 1 country.

Arthur T KopylovDepartment of Pathology, Institute of General Pathology and Pathophysiology, 8 Baltyiskaya str., 125315, Moscow, Russia. a.t.kopylov@gmail.com.ORCID 0000-0002-7199-372X
Olga PapyshevaS.S. Yudin 7th State Clinical Hospital, 4 Kolomenskaya str., 115446, Moscow, Russia.
Iveta GribovaN.E. Bauman 29th State Clinical Hospital, 2 Hospitalnaya sq., 110020, Moscow, Russia.
Galina KotayschN.E. Bauman 29th State Clinical Hospital, 2 Hospitalnaya sq., 110020, Moscow, Russia.
Lubov KharitonovaN.I. Pirogov Medical University, 1 Ostrovityanova st., 117997, Moscow, Russia.
Tatiana MayatskayaN.I. Pirogov Medical University, 1 Ostrovityanova st., 117997, Moscow, Russia.
Ekaterina SokerinaDepartment of Pathology, Institute of General Pathology and Pathophysiology, 8 Baltyiskaya str., 125315, Moscow, Russia.
Anna L KayshevaInstitute of Biomedical Chemistry, Biobanking Group, 10 Pogodinskaya str., 119121, Moscow, Russia.
Sergey G MorozovDepartment of Pathology, Institute of General Pathology and Pathophysiology, 8 Baltyiskaya str., 125315, Moscow, Russia.
Research Institute of General Pathology and Pathophysiology, the Russian Academy of Medical Sciences · RUPirogov Russian National Research Medical University · RUCity Clinical Hospital · RUInstitute of Biomedical Chemistry · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gestational diabetes mellitus is a daunting problem accompanied by severe fetal development complications and type 2 diabetes mellitus in postpartum. Diagnosis of diabetic conditions occurs only in the second trimester, while associated antenatal complications are typically revealed even later. We acquired an assay of peripheral and cord blood samples of patients with different types of diabetes mellitus who delivered either healthy newborns or associated with fetopathy complications. Obtained data were handled with qualitative and quantitative analysis. Pathways of molecular events involved in diabetes mellitus and fetopathy were reconstructed based on the discovered markers and their quantitative alteration. Plenty of pathways were integrated to differentiate the type of diabetes and to recognize the impact of the diabetic condition on fetal development. The impaired triglycerides transport, glucose uptake, and consequent insulin resistance are mostly affected by faulted lipid metabolism (APOM, APOD, APOH, APOC1) and encouraged by oxidative stress (CP, TF, ORM2) and inflammation (CFH, CFB, CLU) as a secondary response accompanied by changes in matrix architecture (AFM, FBLN1, AMBP). Alterations in proteomes of peripheral and cord blood were expectedly unequal. Both up- and downregulated markers were accommodated in the cast of molecular events interconnected with the lipid metabolism, RXR/PPAR-signaling pathway, and extracellular architecture modulation. The obtained results congregate numerous biological processes to molecular events that underline diabetes during gestation and uncover some critical aspects affecting fetal growth and development.

Indexed as

Fetal DevelopmentAdultBiomarkersCase-Control StudiesDiabetes, GestationalDiabetes Mellitus, Type 2FemaleHumansInfant, NewbornInfant, Newborn, DiseasesMass SpectrometryPregnancyPrenatal DiagnosisPrenatal Exposure Delayed EffectsProteomeBiomarkersProteome

Identifiers

PMID33184417
PMCPMC7665025
OpenAlexW3103506970

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.