Evidence map›Paper›PMID 32484253›Full record

ArticleClinical and experimental immunology2020

Abnormal processing of IL-1β in NLRP7-mutated monocytes in hydatidiform mole patients.

P Zhang, X Zhu, X Yu, B Huang, T Jiang, X Zhang, H Yang, J Qian

Erratum issuedOpen access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Clinical and experimental immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 26% 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

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

  1. Molecular Basis of Hydatidiform Moles-A Systematic Review.International journal of molecular sciences · 2024
    Pooled it
  2. Cancers · 2026
    Review
  3. Article
  4. Review
  5. Corrigendum.Clinical and experimental immunology · 2021
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

P ZhangDepartment of Gynecology, The First Affiliated Hospital, Zhejiang University of Medicine School, Zhejiang University, Hangzhou, China.
X ZhuDepartment of Gynecology, The First Affiliated Hospital, Zhejiang University of Medicine School, Zhejiang University, Hangzhou, China.
X YuDepartment of Gynecology, The First Affiliated Hospital, Zhejiang University of Medicine School, Zhejiang University, Hangzhou, China.
B HuangDepartment of Gynecology, The First Affiliated Hospital, Zhejiang University of Medicine School, Zhejiang University, Hangzhou, China.
T JiangDepartment of Gynecology, The First Affiliated Hospital, Zhejiang University of Medicine School, Zhejiang University, Hangzhou, China.
X ZhangDepartment of Pathology, Women's Hospital, Zhejiang University School of Medicine, Hangzhou, China.
H YangDepartment of Pathology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
J QianDepartment of Gynecology, The First Affiliated Hospital, Zhejiang University of Medicine School, Zhejiang University, Hangzhou, China.ORCID 0000-0003-1320-6860
First Affiliated Hospital Zhejiang University · CNWomen's Hospital, School of Medicine, Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NOD-like receptor pyrin 7 (NLRP7) has been identified as the major gene responsible for the recurrent hydatidiform mole (RHM). The immunological role of NLRP7 mutation in HM patients has not been conclusively demonstrated. Hence, we aim to demonstrate this role in our study. We followed 12 new patients with NLRP7 non-synonymous variations (NSVs) from date to date. Peripheral blood mononuclear cells (PBMCs) were collected separately from patients with and without NLRP7 mutation. Supernatant interleukin (IL)-1β secretion, intracellular pro-IL-1β and mature IL-1β expressions were measured after 24 h lipopolysaccharide (LPS) stimulation. Plasmids with corresponding NSVs were generated to evaluate the ability of processing pro-IL-1β into mature IL-1β in vitro. Homozygous or compound heterozygous NLRP7 mutations secreted less IL-1β in roots of abnormal intracellular pro-IL-1β or mature IL-1β, according to different domains. Plasmids with NSVs could also affect processing or/and trafficking together with caspase-1 and apoptosis-associated speck-like protein (ASC). Inflammasome-related NLRP7 mutation is a potential mechanism of RHM.

Indexed as

Adaptor Proteins, Signal TransducingHydatidiform MoleInterleukin-1betaMutationNeoplasm ProteinsAdultFemaleFollow-Up StudiesHEK293 CellsHumansLeukocytes, MononuclearPregnancyAdaptor Proteins, Signal TransducingIL1B protein, humanInterleukin-1betaNeoplasm ProteinsNLRP7 protein, humanhydatidiform moleIL-1βNLRP7

Identifiers

PMID32484253
PMCPMC7488120
OpenAlexW3031931535

What OpenQuestion holds

Textmetadata
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.