Genetic drivers of congenital cardiac fibrosis.

Abstract readReview

In one paragraph

Review in Communications biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it

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

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

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

2 authors.

Angela C ZeiglerUCLA David Geffen School of Medicine, Neonatal Congenital Heart Laboratory, 675 Charles E. Young Drive, MRL Building Laboratory 3447/3457, Los Angeles, CA, USA.ORCID 0000-0002-7142-9459

Marlin ToumaUCLA David Geffen School of Medicine, Neonatal Congenital Heart Laboratory, 675 Charles E. Young Drive, MRL Building Laboratory 3447/3457, Los Angeles, CA, USA. mtouma@mednet.ucla.edu.ORCID 0000-0002-2827-4068

Funding

Novel Gene-Environment Regulatory Circuit in Chamber-Specific Growth of Perinatal HeartR01HL153853 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TOUMA, MARLIN · 2020 to 2023

$1.6M

NHLBI NIH HHS R01 HL153853UC | University of California, Los Angeles (UCLA) Academic Senate Faculty Research FundUnited States Department of Defense | Biometrics Identity Management Agency (BIMA) Idea Development Award HT9425-25-1-0763 Project Number: MD240028U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI) NIH/1R01 HL153853

6 · The paper itself

Abstract

Cardiac fibrosis in congenital heart disease (CHD) is associated with poor outcomes, but the genetic risk factors have not been clearly outlined. This review details genes important for regulation of normal cardiac development or fibrosis, particularly cilia-related genes. Specific CHD pathologies have different patterns of fibrosis, likely from interaction between genetic mutations and environmental factors. Future studies are more feasible as tools like single-cell RNAseq and patient-derived organoids have become more affordable and easier to implement. A better understanding of genetic risk factors for fibrosis in CHD could improve diagnosis and treatment for these patients.

Indexed as

Heart Defects, CongenitalMyocardiumAnimalsFibrosisGenetic Predisposition to DiseaseHumansMutationRisk Factors

Identifiers

PMID42203827

DOI10.1038/s42003-026-10353-2

PMCPMC13216529

What OpenQuestion holds

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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.