Evidence map›Paper›PMID 35310974›Full record

ReviewFrontiers in cardiovascular medicine2022

Complement C1q Binding Protein (C1QBP): Physiological Functions, Mutation-Associated Mitochondrial Cardiomyopathy and Current Disease Models.

Jie Wang, Christopher L-H Huang, Yanmin Zhang

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cardiovascular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

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  9. Novel cuproptosis-related genesOpen life sciences · 2025
    Article
  10. Review
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  12. Identification ofFrontiers in molecular biosciences · 2024
    Article
  13. Transcriptomic response of lumpfish (Frontiers in immunology · 2024
    Article
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  16. Review
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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

3 authors at 3 institutions in 2 countries.

Jie WangNational Regional Children's Medical Center (Northwest), Xi'an, China.
Christopher L-H HuangPhysiological Laboratory, University of Cambridge, Cambridge, United Kingdom.
Yanmin ZhangNational Regional Children's Medical Center (Northwest), Xi'an, China.
Northwest Women's and Children's Hospital · CNPhysiological Society · GBXi'an Institute of Optics and Precision Mechanics · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Complement C1q binding protein (C1QBP, p32) is primarily localized in mitochondrial matrix and associated with mitochondrial oxidative phosphorylative function. C1QBP deficiency presents as a mitochondrial disorder involving multiple organ systems. Recently, disease associated C1QBP mutations have been identified in patients with a combined oxidative phosphorylation deficiency taking an autosomal recessive inherited pattern. The clinical spectrum ranges from intrauterine growth restriction to childhood (cardio) myopathy and late-onset progressive external ophthalmoplegia. This review summarizes the physiological functions of C1QBP, its mutation-associated mitochondrial cardiomyopathy shown in the reported available patients and current experimental disease platforms modeling these conditions.

Indexed as

C1QPBcombined oxidative phosphorylation deficiencydisease modelsmitochondrial cardiomyopathiesmutationphysiological functions

Identifiers

PMID35310974
PMCPMC8924301
OpenAlexW4214891154

What Socratic 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 Socratic graph.