Evidence map›Paper›PMID 39000360›Full record

ArticleInternational journal of molecular sciences2024

Deletion of the Mitochondrial Membrane Protein Fam210b Is Associated with the Development of Systemic Lupus Erythematosus.

Yaqi Xu, Ran Gao, Min Zhang, Qi Zeng, Gaizhi Zhu, Jinming Qiu, Wenting Su, Renxi Wang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

8 authors.

Yaqi XuBeijing Institute of Brain Disorders, Laboratory of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Capital Medical University, No. 10 Xitoutiao, You An Men, Beijing 100069, China.ORCID 0000-0002-5351-3315
Ran GaoBeijing Institute of Brain Disorders, Laboratory of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Capital Medical University, No. 10 Xitoutiao, You An Men, Beijing 100069, China.
Min ZhangBeijing Institute of Brain Disorders, Laboratory of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Capital Medical University, No. 10 Xitoutiao, You An Men, Beijing 100069, China.
Qi ZengBeijing Institute of Brain Disorders, Laboratory of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Capital Medical University, No. 10 Xitoutiao, You An Men, Beijing 100069, China.
Gaizhi ZhuBeijing Institute of Brain Disorders, Laboratory of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Capital Medical University, No. 10 Xitoutiao, You An Men, Beijing 100069, China.
Jinming QiuBeijing Institute of Brain Disorders, Laboratory of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Capital Medical University, No. 10 Xitoutiao, You An Men, Beijing 100069, China.
Wenting SuBeijing Institute of Brain Disorders, Laboratory of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Capital Medical University, No. 10 Xitoutiao, You An Men, Beijing 100069, China.
Renxi WangBeijing Institute of Brain Disorders, Laboratory of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Capital Medical University, No. 10 Xitoutiao, You An Men, Beijing 100069, China.ORCID 0000-0003-4130-3334

Funding

National Natural Science Foundation of China 82071758 and 32270933R&D Program of Beijing Municipal Education Commission KZ202210025035
6 · The paper itself

Abstract

Mitochondrial dysfunction has been increasingly recognized as a trigger for systemic lupus erythematosus (SLE). Recent bioinformatics studies have suggested Fam210b as a significant candidate for the classification and therapeutic targeting of SLE. To experimentally prove the role of Fam210b in SLE, we constructed

Indexed as

Lupus Erythematosus, SystemicMice, KnockoutAnimalsAntibodies, AntinuclearDisease Models, AnimalErythroid CellsFemaleImmunoglobulin GMembrane ProteinsMiceMice, Inbred C57BLMitochondrial MembranesMitochondrial ProteinsReactive Oxygen SpeciesSpleenAntibodies, AntinuclearImmunoglobulin GMembrane ProteinsMitochondrial ProteinsReactive Oxygen Speciesautoantibodyerythroid cellsFam210bsingle-cell sequencingsystemic lupus erythematosus

Identifiers

PMID39000360
PMCPMC11241391

What OpenQuestion holds

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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.