Evidence map›Paper›PMID 40569905›Full record

ArticlePloS one2025

Rare and novel variant load threshold for KIF7, GJA1 and PDE1C genes elevates the risk of severity of congenital heart defects in Down syndrome.

Agnish Ganguly, Samudra Pal, Srilagna Chatterjee, Madhusudan Das, Sumantra Sarkar, Sujay Ghosh

Abstract read
In one paragraph

Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

6 authors.

Agnish GangulyCytogenetics-Genomics and Down syndrome Research Unit, Department of Zoology, University of Calcutta, Kolkata, West Bengal, India.
Samudra PalCytogenetics-Genomics and Down syndrome Research Unit, Department of Zoology, University of Calcutta, Kolkata, West Bengal, India.
Srilagna ChatterjeeDepartment of Zoology, University of Calcutta, Kolkata, West Bengal, India.
Madhusudan DasDepartment of Zoology, University of Calcutta, Kolkata, West Bengal, India.
Sumantra SarkarDepartment of Pediatric Medicine, Diamond Harbour Government Medical College & Hospital, Diamond Harbour, West Bengal, India.
Sujay GhoshCytogenetics-Genomics and Down syndrome Research Unit, Department of Zoology, University of Calcutta, Kolkata, West Bengal, India.ORCID 0000-0003-1703-8446

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Individuals with Down syndrome (DS) exhibit a higher incidence of congenital heart defects (CHD). The objective of the present study was to investigate ethnicity-specific genetic variants that increase the risk of CHD in children with DS from the Indian Bengali population. We conducted whole exome sequencing of the genomes of Down syndrome children with and without CHD and subsequently tested the identified variants in a larger cohort (N = 1798). Our findings revealed two rare variants, KIF7 rs138354681 and GJA1 rs778110855, as well as one novel variant, PDE1C PP785745, present in children with DS and CHD but absent in those without CHD. In-silico analyses indicated that these variants are pathogenic. The frequencies of the heterozygous genotypes for KIF7 rs138354681, GJA1 rs778110855, and PDE1C PP785745 were recorded as 0.027, 0.016, and 0.032, respectively. Among the 31 carriers identified, 18 individuals exhibited two variants, while four were found to have three co-occurring variants. The majority of these individuals required surgical intervention for correction, in contrast to single variant carriers, of whom only three out of nine needed surgeries. A polygenic risk score analysis revealed higher score to be significantly associated with both the presence of multiple variants and the subsequent need for surgical correction. We hypothesise that the synergistic effects of multiple variants heighten the severity of CHD, particularly in cases of ventricular septal defects, thereby necessitating surgical correction. These findings significantly enhance our understanding of the unique population-specific aetiology of CHD and the basis for the severity of its clinical presentation in individuals with Down syndrome.

Indexed as

Connexin 43Cyclic Nucleotide Phosphodiesterases, Type 1Down SyndromeHeart Defects, CongenitalKinesinsChildChild, PreschoolExome SequencingFemaleGenetic Predisposition to DiseaseHumansInfantMalePolymorphism, Single NucleotideConnexin 43Cyclic Nucleotide Phosphodiesterases, Type 1GJA1 protein, humanKinesins

Identifiers

PMID40569905
PMCPMC12200707

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.