Evidence mapPaperPMID 42305007Full record

SynthesisZhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics2026

[Advances in the molecular genetics of nuclear gene mutations causing pediatric mitochondrial cardiomyopathy].

Zi-Wei Wang, Yu-Qi Wang, Chun-Li Wang

Abstract readEnglish AbstractSystematic Review
In one paragraph

Synthesis in Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

What it found

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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Zi-Wei WangDepartment of Cardiology, Children's Hospital of Nanjing Medical University, Nanjing 210008, China.
Yu-Qi WangDepartment of Cardiology, Children's Hospital of Nanjing Medical University, Nanjing 210008, China.
Chun-Li Wang

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial cardiomyopathy (MCM) is a heterogeneous group of disorders characterized by abnormal myocardial structure and/or function caused by defects in genes encoding the oxidative phosphorylation chain. This review systematically summarizes molecular genetic advances regarding nuclear gene mutations associated with pediatric MCM, focusing on mutations affecting pathways including respiratory chain complex subunits and assembly factors, coenzyme Q10 biosynthesis, mitochondrial DNA maintenance and expression, lipid metabolism, iron-sulfur cluster metabolism, apoptosis regulation, and mitochondrial dynamics. These nuclear gene mutations contribute to myocardial pathological changes by disrupting key processes such as mitochondrial energy metabolism, membrane stability, and signal transduction. The review provides a theoretical basis for precise clinical diagnosis and the exploration of potential molecular targets in pediatric MCM.

Indexed as

CardiomyopathiesCell NucleusChildDNA, MitochondrialGene Expression RegulationHeart Defects, CongenitalHumansLipid MetabolismMitochondrial DiseasesMolecular BiologyMutationOxidative PhosphorylationUbiquinonecoenzyme Q10DNA, MitochondrialUbiquinoneChildMitochondrial cardiomyopathyMutationNuclear geneOxidative phosphorylation

Identifiers

PMID42305007
PMCPMC13273480

What Socratic holds

Textmetadata
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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 Socratic graph.