Evidence map›Paper›PMID 37386367›Full record

ArticleMolecular medicine (Cambridge, Mass.)2023

Calcium/calmodulin dependent protein kinase IV in trophoblast cells under insulin resistance: functional and metabolomic analyses.

Ling Li, Li Li, Ying Shao, Runyu Du, Ling Li, Xiaoguang Shi, Yu Bai

Abstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
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

8 citing papers in PubMed.

  1. Article
  2. Integrative Transcriptomic and Proteomic Analysis RevealsAnimals : an open access journal from MDPI · 2025
    Article
  3. Article
  4. Review
  5. Article
  6. The Roles of Obesity and ASB4 in Preeclampsia Pathogenesis.International journal of molecular sciences · 2024
    Review
  7. Article
  8. 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

7 authors.

Ling LiDepartment of Endocrinology, Shengjing Hospital of China Medical University, 36 Sanhao Street, Shenyang, 110004, Liaoning, People's Republic of China.
Li LiDepartment of Endocrinology, Shengjing Hospital of China Medical University, 36 Sanhao Street, Shenyang, 110004, Liaoning, People's Republic of China.
Ying ShaoDepartment of Endocrinology, Shengjing Hospital of China Medical University, 36 Sanhao Street, Shenyang, 110004, Liaoning, People's Republic of China.
Runyu DuDepartment of Endocrinology, Shengjing Hospital of China Medical University, 36 Sanhao Street, Shenyang, 110004, Liaoning, People's Republic of China.
Ling LiDepartment of Endocrinology, Shengjing Hospital of China Medical University, 36 Sanhao Street, Shenyang, 110004, Liaoning, People's Republic of China.
Xiaoguang ShiDepartment of Endocrinology, Shengjing Hospital of China Medical University, 36 Sanhao Street, Shenyang, 110004, Liaoning, People's Republic of China. shixg@sj-hospital.org.
Yu BaiDepartment of Endocrinology, Shengjing Hospital of China Medical University, 36 Sanhao Street, Shenyang, 110004, Liaoning, People's Republic of China. baiyunfm@hotmail.com.ORCID 0000-0002-2737-6038

Funding

Doctoral Start-up Foundation of Liaoning Province 20071053Hospital Project Fund of Shengjing Hospital of China Medical University M1050Scientific Research Foundation for the Returned Overseas Chinese Scholars, State Education Ministry 2010-1174
6 · The paper itself

Abstract

backgroundInsulin resistance (IR) is an important determinant of glucose metabolic disturbance and placental dysplasia in gestational diabetes mellitus (GDM). Calcium/calmodulin dependent protein kinase IV (CAMK4) improves insulin IR induced by a high-fat diet (HFD). The current study sought to elucidate the role and potential mechanism of CAMK4 in GDM.

methodsA GDM model was established in female C57BL/6J mice via HFD feeding for one week before mating and throughout gestation. The IR was elicited by 10

resultsDecreased CAMK4 expression was found in the placenta of GDM mice. CAMK4 overexpression ameliorated IR-induced viability impairment, migratory and invasive capacity inhibition, autophagy blocking, insulin signaling inactivation and glucose uptake disorder in trophoblast cells. CAMK4 also transcriptionally activated orphan nuclear receptor NUR77, and the effects of CAMK4 were abrogated by silencing of NUR77. Metabolomics analysis revealed that CAMK4 overexpression caused alterations of amino acid, lipid and carbohydrate metabolism, which were important in GDM.

conclusionOur results indicated that CAMK4/NUR77 axis may provide novel potential targets in GDM treatment.

Indexed as

Diabetes, GestationalInsulin ResistanceInsulinsAnimalsCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 4FemaleHumansMetabolomicsMiceMice, Inbred C57BLPlacentaPregnancyTrophoblastsCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 4CAMK4 protein, humanInsulinsAutophagyCalcium/calmodulin dependent protein kinase IVGestational diabetes mellitusInsulin resistancemetabolomicsTrophoblast cells

Identifiers

PMID37386367
PMCPMC10308755

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Registered trials

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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.