Evidence map›Paper›PMID 37511352›Full record

ArticleInternational journal of molecular sciences2023

Single Cell Transcriptomic Analysis in a Mouse Model of Barth Syndrome Reveals Cell-Specific Alterations in Gene Expression and Intercellular Communication.

Gayani Perera, Liam Power, Amy Larson, Christina J Codden, Junya Awata, Rebecca Batorsky, Douglas Strathdee, Michael T Chin

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. Single Cell Transcriptomic Profiling ofJournal of the American Heart Association · 2025
    Article
  3. Article
  4. A Barth Syndrome Patient-DerivedInternational journal of molecular sciences · 2024
    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 at 3 institutions in 2 countries.

Gayani PereraMolecular Cardiology Research Institute, Tufts Medical Center, Boston, MA 02111, USA.
Liam PowerMedical Scientist Training Program, Tufts University School of Medicine, Boston, MA 02111, USA.ORCID 0000-0002-3402-8429
Amy LarsonMolecular Cardiology Research Institute, Tufts Medical Center, Boston, MA 02111, USA.ORCID 0000-0002-5217-3347
Christina J CoddenMolecular Cardiology Research Institute, Tufts Medical Center, Boston, MA 02111, USA.
Junya AwataMolecular Cardiology Research Institute, Tufts Medical Center, Boston, MA 02111, USA.
Rebecca BatorskyData Intensive Studies Center, Tufts University, Medford, MA 02155, USA.ORCID 0000-0003-4712-6500
Douglas StrathdeeCancer Research UK Beatson Institute, Glasgow G61 1BD, UK.
Michael T ChinMolecular Cardiology Research Institute, Tufts Medical Center, Boston, MA 02111, USA.ORCID 0000-0003-3065-8498
Tufts Medical Center · USTufts University · USCancer Research UK Scotland Institute · GB

Funding

MEDICAL SCIENTIST TRAINING PROGRAM AT TUFTS UNIVERSITYT32GM008448 · NIGMS · TUFTS UNIVERSITY BOSTON · PI CHIN, MICHAEL T · 1994 to 2022
$9.1M
Tafazzin and metabolic reprogramming during cardiomyopathyR01HL159436 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI CONWAY, SIMON JAMES · 2021 to 2024
$2.3M
Functional assay development for tafazzin enzyme replacement candidate selectionR33HL154137 · NHLBI · TUFTS MEDICAL CENTER · PI CHIN, MICHAEL T · 2023 to 2023
$623k
Cancer Research UK SICR_CORE_TRANST_2324NHLBI NIH HHS R01 HL159436NHLBI NIH HHS R33 HL154137NIGMS NIH HHS T32 GM008448
6 · The paper itself

Abstract

Barth Syndrome, a rare X-linked disorder affecting 1:300,000 live births, results from defects in Tafazzin, an acyltransferase that remodels cardiolipin and is essential for mitochondrial respiration. Barth Syndrome patients develop cardiomyopathy, muscular hypotonia and cyclic neutropenia during childhood, rarely surviving to middle age. At present, no effective therapy exists, and downstream transcriptional effects of Tafazzin dysfunction are incompletely understood. To identify novel, cell-specific, pathological pathways that mediate heart dysfunction, we performed single-nucleus RNA-sequencing (snRNA-seq) on wild-type (WT) and

Indexed as

Barth SyndromeCardiomyopathiesAcyltransferasesAnimalsCardiolipinsCell CommunicationDisease Models, AnimalEndothelial CellsLigandsMiceMice, KnockoutTranscriptomeAcyltransferasesCardiolipinsLigandsBarth Syndromecardiomyopathygene expressionmetabolismmitochondriasingle-nucleus RNA sequencingTafazzin

Identifiers

PMID37511352
PMCPMC10380964
OpenAlexW4384825199

What OpenQuestion 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 OpenQuestion graph.