Evidence map›Paper›PMID 40863384›Full record

ArticleJournal of cardiovascular development and disease2025

Dysfunctional Electron Transport Chain Assembly in COXPD8.

Gisela Beutner, Heidie L Huyck, Gail Deutsch, Gloria S Pryhuber, George A Porter

Abstract read
In one paragraph

Article in Journal of cardiovascular development and disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed, 1 pooled it
–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 synthesis or guideline pooled it.

  1. [Advances in the molecular genetics of nuclear gene mutations causing pediatric mitochondrial cardiomyopathy].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2026
    Pooled it
  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

5 authors.

Gisela BeutnerDepartment of Pediatrics-Division Cardiology, University of Rochester Medical Center, Rochester, NY 14642, USA.ORCID 0000-0002-6157-0934
Heidie L HuyckDepartment of Pediatrics-Division of Neonatology, University of Rochester Medical Center, Rochester, NY 14642, USA.
Gail DeutschDepartment of Pathology, Seattle Children's Hospital and University of Washington Medical Center, Seattle, WA 98101, USA.
Gloria S PryhuberDepartment of Pediatrics-Division of Neonatology, University of Rochester Medical Center, Rochester, NY 14642, USA.ORCID 0000-0002-9185-3994
George A PorterDepartment of Pediatrics-Division Cardiology, University of Rochester Medical Center, Rochester, NY 14642, USA.ORCID 0000-0003-0726-9988

Funding

The University of Rochester's Clinical and Translational Science InstituteUL1TR002001 · NCATS · UNIVERSITY OF ROCHESTER · PI WILSON, KAREN M., ZAND, MARTIN S · 2016 to 2024
$34.6M
BioRepository for INvestigation of Diseases of the Lung (BRINDL) - Phase IIIU01HL148861 · NHLBI · UNIVERSITY OF ROCHESTER · PI GLORIA S PRYHUBER · 2019 to 2026
$9.7M
Biorepository for Investigation of Neonatal Diseases of Lung-Normal (BRINDL-NL)U01HL122700 · NHLBI · UNIVERSITY OF ROCHESTER · PI PRYHUBER, GLORIA S · 2014 to 2018
$6.1M
Cyclophilin D Regulates Neonatal Cardiac Bioenergetics and FunctionR01HL144776 · NHLBI · UNIVERSITY OF ROCHESTER · PI PORTER, GEORGE A · 2019 to 2022
$2.0M
NCATS NIH HHS UL1 TR002001NHLBI NIH HHS R01 HL144776NHLBI NIH HHS U01 HL122700NHLBI NIH HHS U01 HL148861NIH HHS 1R01HL144776-05NIH HHS 1U01HL122700-06NIH HHS 1U01HL148861-05NIH HHS UL1 TR002001-05
6 · The paper itself

Abstract

Combined oxidative phosphorylation deficiency type 8 (COXPD8) is an autosomal recessive mitochondrial disorder caused by a mutation of the nuclear encoded mitochondrial alanyl-tRNA synthetase gene (AARS2). Clinical manifestations of COXPD8 include lethal infantile hypertrophic cardiomyopathy, pulmonary hypoplasia, generalized muscle weakness, and neurological involvement. We report a patient with COXPD8 caused by two mutations in the AARS2 gene. The c.1738 C>G mutation has not been previously reported, while the c.2872 C>T mutation has been associated with pulmonary hypoplasia and hypertrophic cardiomyopathy. Cardiac tissue, obtained through the LungMAP program, showed that, compared to other patients of similar ages, these two mutations affect not only the assembly of functional monomeric complexes (Cx) I and IV of the electron transport chain (ETC) but also limit the formation of respiratory supercomplexes. This patient had altered expression of some ETC proteins but normal expression of several enzymes of the tricarboxylic acid cycle. We also show that one of the control/comparison patients had an undiagnosed ETC Cx IV deficiency. In conclusion, our data demonstrate that the two mutations of the AARS2 gene are associated with failed assembly of Cx I and Cx IV and reduced formation of respiratory supercomplexes of the ETC, likely leading to acute bioenergetic stress.

Indexed as

COXPD8electron transport chainhypertrophic cardiomyopathymitochondrial diseasemitochondrial supercomplexes

Identifiers

PMID40863384
PMCPMC12386341

What OpenQuestion holds

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Registered trials

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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.