Evidence map›Paper›PMID 39472874›Full record

ArticleBMC pregnancy and childbirth2024

Impact of Vitamin D deficiency on immunological and metabolic responses in women with recurrent pregnancy loss: focus on VDBP/HLA-G1/CTLA-4/ENTPD1/adenosine-fetal-maternal conflict crosstalk.

Aisha Nawaf Al Balawi, Noaf Abdullah N Alblwi, Riham Soliman, Ali H El-Far, Mervat G Hassan, Tarek El-Sewedy, Fuad Ameen, Nadia F Ismail, Alaa Elmetwalli

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC pregnancy and childbirth, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. 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

9 authors.

Aisha Nawaf Al BalawiBiology Department, University College of Haql, University of Tabuk, Tabuk, Saudi Arabia. an.albalawi@ut.edu.sa.
Noaf Abdullah N AlblwiDepartment of Nursing, Al Hadithah General Hospital, Al Qurayyat, Saudi Arabia.
Riham SolimanTropical Medicine Department, Faculty of Medicine, Port Said University, Port Said, Egypt.
Ali H El-FarKey Laboratory of Epigenetics and Oncology, The Research Center for Preclinical Medicine, Southwest Medical University, Luzhou, 646000, China.
Mervat G HassanDepartment of Botany and Microbiology, Faculty of Science, Benha University, Benha, 13511, Egypt.
Tarek El-SewedyDepartment of Applied Medical Chemistry, Medical Research Institute, Alexandria University, Alexandria, Egypt.
Fuad AmeenDepartment of Botany and Microbiology, College of Science, King Saud University, 11451, Riyadh, Saudi Arabia.
Nadia F IsmailHealth Information Management Program, Biochemistry, Faculty of Health Science Technology, Borg El Arab Technological University, Alexandria, Egypt.
Alaa ElmetwalliDepartment of Clinical Trial Research Unit and Drug Discovery, Egyptian Liver Research Institute and Hospital (ELRIAH), Mansoura, Egypt. dr.prof2011@gmail.com.ORCID http://orcid.org/0000-0001-5372-4297

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimRecurrent pregnancy loss (RPL), also known as recurrent implantation failure (RIF), is a distressing condition affecting women characterized by two or more consecutive miscarriages or the inability to carry a pregnancy beyond 20 weeks. Immunological factors and genetic variations, particularly in Vit D Binding Protein (VDBP), have gained attention as potential contributors to RPL. This study aimed to provide insight into the immunological, genetic, and metabolic networks underlying RPL, placing a particular emphasis on the interactions between VDBP, HLA-G1, CTLA-4, ENTPD1, and adenosine-fetal-maternal conflict crosstalk.

methodsA retrospective study included 198 women with three or more consecutive spontaneous abortions. Exclusion criteria comprised uterine abnormalities, endocrine disorders, parental chromosomal abnormalities, infectious factors, autoimmune diseases, or connective tissue diseases. Immunological interplay was investigated in 162 female participants, divided into two groups based on their Vit D levels: normal Vit D-RPL and low Vit D-RPL. Various laboratory techniques were employed, including LC/MS/MS for Vit D measurement, ELISA for protein detection, flow cytometry for immune function analysis, and molecular docking for protein-ligand interaction assessment.

resultsGeneral characteristics between groups were significant regarding Vit D and glucose levels. Low Vit D levels were associated with decreased NK cell activity and downregulation of HLA-G1 and HLA-G5 proteins, while CTLA-4 revealed upregulation. VDBP was significantly downregulated in the low Vit D group. Our findings highlight the intricate relationship between Vit D status and adenosine metabolism by the downregulation of SGLT1, and NT5E, key components of adenosine metabolism, suggests that Vit D deficiency may disrupt the regulation of adenosine levels, leading to an impaired reproductive outcome. HNF1β, a negative regulator of VDBP, was upregulated, while HNF1α, a positive regulator, was downregulated in low Vit D women after RPL. Molecular docking analysis revealed crucial residues involved in the interaction between Vit D and HNF1β.

conclusionCollectively, these findings underscore the importance of Vit D in modulating immune function and molecular pathways relevant to pregnancy maintenance, highlighting the need for further research to elucidate the mechanisms and potential therapeutic interventions for improving pregnancy outcomes in individuals with Vit D deficiency and RPL.

Indexed as

Abortion, HabitualAdenosineCTLA-4 AntigenHLA-G AntigensVitamin D DeficiencyAdultFemaleHumansMolecular Docking SimulationPregnancyProgrammed Cell Death 1 ReceptorRetrospective StudiesVitamin DVitamin D-Binding ProteinAdenosineCTLA-4 AntigenCTLA4 protein, humanGC protein, humanHLA-G AntigensProgrammed Cell Death 1 ReceptorVitamin DVitamin D-Binding ProteinCTLA-4 AntigenFetal-maternal conflictGenetic variationRecurrent pregnancy lossVitamin D-Binding protein

Identifiers

PMID39472874
PMCPMC11523824

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.