ArticleiScience2023
Interferon hyperactivity impairs cardiogenesis in Down syndrome via downregulation of canonical Wnt signaling.
Article in iScience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Revisiting down syndrome through the lens of interferonopathy and innate immune dysregulation.Frontiers in immunology · 2026Pooled it
- Trial
- Fasudil induces anti-inflammatory transcriptomic changes and increased proliferation in human trisomy 21 neural progenitor cells.Biology open · 2026Article
- Immune dysregulation in children with Down syndrome: clinical implications and emerging therapies.Current opinion in rheumatology · 2026Review
- A Researcher's guide to rodent models of Down syndrome: Recent insights and translational perspectives.STAR protocols · 2026Review
- Distinct roles of the JADE and BRPF scaffolding subunits of the acetyltransferase HBO1 complex.Nature communications · 2026Article
- Systematic multi-omic deconvolution of the clinical heterogeneity of Down syndrome.Nature communications · 2026Article
- Anti-inflammatory and pro-proliferative effects of fasudil in human trisomy 21 neural progenitor cells.bioRxiv : the preprint server for biology · 2026Article
- The Wnt/β-catenin pathway maintains homeostasis of amniocytes in Down syndrome.BMC molecular and cell biology · 2026Article
- Altered hepatic metabolism in Down syndrome.Cell reports · 2026Article
- Prevention of Respiratory Infections in Children with Congenital Heart Disease: Current Evidence and Clinical Strategies.Vaccines · 2025Review
- The placental effects of trisomy for human chromosome 21 orthologs in four mouse models of Down syndrome.Biology open · 2025Article
- Generation of human induced pluripotent stem cell lines from a fetus with congenital long QT syndrome and her healthy parents.Stem cell research · 2025Article
- Article
- The Opportunities and Challenges in the Molecular Mechanism Research of Congenital Heart Disease: A Review.Molecular syndromology · 2025Review
- JAK inhibition decreases the autoimmune burden in Down syndrome.medRxiv : the preprint server for health sciences · 2024Article
- Differentiation of Pluripotent Stem Cells for Disease Modeling: Learning from Heart Development.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Review
- Exploring the origins of neurodevelopmental proteasomopathies associated with cardiac malformations: are neural crest cells central to certain pathological mechanisms?Frontiers in cell and developmental biology · 2024Article
- Integration of ATAC-seq and RNA-seq identifies MX1-mediated AP-1 transcriptional regulation as a therapeutic target for Down syndrome.Biological research · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Congenital heart defects (CHDs) are frequent in children with Down syndrome (DS), caused by trisomy of chromosome 21. However, the underlying mechanisms are poorly understood. Here, using a human-induced pluripotent stem cell (iPSC)-based model and the Dp(16)1Yey/+ (Dp16) mouse model of DS, we identified downregulation of canonical Wnt signaling downstream of increased dosage of interferon (IFN) receptors (IFNRs) genes on chromosome 21 as a causative factor of cardiogenic dysregulation in DS. We differentiated human iPSCs derived from individuals with DS and CHDs, and healthy euploid controls into cardiac cells. We observed that T21 upregulates IFN signaling, downregulates the canonical WNT pathway, and impairs cardiac differentiation. Furthermore, genetic and pharmacological normalization of IFN signaling restored canonical WNT signaling and rescued defects in cardiogenesis in DS
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.