Evidence map›Paper›PMID 30336561›Full record

ReviewInternational journal of molecular sciences2018

Heat Shock Proteins as a Potential Therapeutic Target in the Treatment of Gestational Diabetes Mellitus: What We Know so Far.

Katarzyna E Skórzyńska-Dziduszko, Żaneta Kimber-Trojnar, Jolanta Patro-Małysza, Agnieszka Stenzel-Bembenek, Jan Oleszczuk, Bożena Leszczyńska-Gorzelak

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

10 citing papers in PubMed, 10 citations in OpenAlex.

  1. Insulin Resistance and Inflammation.International journal of molecular sciences · 2026
    Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Novel Biomolecules in the Pathogenesis of Gestational Diabetes Mellitus 2.0.International journal of molecular sciences · 2022
    Review
  7. Novel Biomolecules in the Pathogenesis of Gestational Diabetes Mellitus.International journal of molecular sciences · 2021
    Review
  8. Review
  9. Review
  10. 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

6 authors at 1 institution in 1 country.

Katarzyna E Skórzyńska-DziduszkoDepartment of Human Physiology, Medical University of Lublin, Radziwillowska 11 Street, 20-080 Lublin, Poland. katarzyna.skorzynska-dziduszko@umlub.pl.ORCID 0000-0002-8718-1187
Żaneta Kimber-TrojnarDepartment of Obstetrics and Perinatology, Medical University of Lublin, K. Jaczewskiego 8 Street, 20-954 Lublin, Poland. zkimber@poczta.onet.pl.ORCID 0000-0001-7295-0409
Jolanta Patro-MałyszaDepartment of Obstetrics and Perinatology, Medical University of Lublin, K. Jaczewskiego 8 Street, 20-954 Lublin, Poland. jolapatro@wp.pl.ORCID 0000-0002-4118-7698
Agnieszka Stenzel-BembenekDepartment of Biochemistry and Molecular Biology, Medical University of Lublin, W. Chodźki 1 Street, 20-093 Lublin, Poland. astenn@wp.pl.
Jan OleszczukDepartment of Obstetrics and Perinatology, Medical University of Lublin, K. Jaczewskiego 8 Street, 20-954 Lublin, Poland. jan.oleszczuk@umlub.pl.
Bożena Leszczyńska-GorzelakDepartment of Obstetrics and Perinatology, Medical University of Lublin, K. Jaczewskiego 8 Street, 20-954 Lublin, Poland. bozena.leszczynska-gorzelak@umlub.pl.
Medical University of Lublin · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gestational diabetes mellitus (GDM) is a complex condition that involves a variety of pathological mechanisms, including pancreatic β-cell failure, insulin resistance, and inflammation. There is an increasing body of literature suggesting that these interrelated phenomena may arise from the common mechanism of endoplasmic reticulum (ER) stress. Both obesity-associated nutrient excess and hyperglycemia disturb ER function in protein folding and transport. This results in the accumulation of polypeptides in the ER lumen and impairs insulin secretion and signaling. Exercise elicits metabolic adaptive responses, which may help to restore normal chaperone expression in insulin-resistant tissues. Pharmacological induction of chaperones, mimicking the metabolic effect of exercise, is a promising therapeutic tool for preventing GDM by maintaining the body's natural stress response. Metformin, a commonly used diabetes medication, has recently been identified as a modulator of ER-stress-associated inflammation. The results of recent studies suggest the potential use of chemical ER chaperones and antioxidant vitamins as therapeutic interventions that can prevent glucose-induced ER stress in GDM placentas. In this review, we discuss whether chaperones may significantly contribute to the pathogenesis of GDM, as well as whether they can be a potential therapeutic target in GDM treatment.

Indexed as

Molecular Targeted TherapyAnimalsDiabetes, GestationalEndoplasmic Reticulum StressFemaleHeat-Shock ProteinsHumansInsulinPregnancyUnfolded Protein ResponseHeat-Shock ProteinsInsulinchaperonesendoplasmic reticulum stressgestational diabetes mellitusheat shock proteinshyperglycemiainflammationinsulin resistancemetformintype 2 diabetes mellitus

Identifiers

PMID30336561
PMCPMC6213996
OpenAlexW2897551311

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.