ArticleCell reports2021
Prenatal correction of IGF2 to rescue the growth phenotypes in mouse models of Beckwith-Wiedemann and Silver-Russell syndromes.
Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 17 citations in OpenAlex.
- Insulin-like growth factor receptor signaling in physiology and disease.Signal transduction and targeted therapy · 2026Review
- Paradoxical regulation of IGF2 in promoting lipid metabolism in adipose tissues.Communications biology · 2025Article
- Generation of live mice from haploid ESCs with germline-DMR deletions or switch.Cell discovery · 2025Article
- Skeletal stem/progenitor cell-derived rather than osteoblast-derived IGF2 supports the development and homeostasis of skeletal system via STAT3.International journal of biological sciences · 2025Article
- Future in the past: paternal reprogramming of offspring phenotype and the epigenetic mechanisms.Archives of toxicology · 2024Review
- Review
- Insulin signaling in development.Development (Cambridge, England) · 2023Article
- Establishment of paternal methylation imprint at theScience advances · 2023Article
- Widespread allele-specific topological domains in the human genome are not confined to imprinted gene clusters.Genome biology · 2023Article
- Epigenetic control and genomic imprinting dynamics of the Dlk1-Dio3 domain.Frontiers in cell and developmental biology · 2023Review
- Overexpression of IGF2 affects mouse weight and glycolipid metabolism and IGF2 is positively related to macrosomia.Frontiers in endocrinology · 2023Article
- DysregulatedeLife · 2022Article
- Association of Parental Factors and Insulin-like Growth Factor 2 Polymorphism with Intrauterine Growth Restriction.Children (Basel, Switzerland) · 2022Article
- Case report: A novelFrontiers in pediatrics · 2022Article
- Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Beckwith-Wiedemann syndrome (BWS) and Silver-Russell syndrome (SRS) are imprinting disorders manifesting as aberrant fetal growth and severe postnatal-growth-related complications. Based on the insulator model, one-third of BWS cases and two-thirds of SRS cases are consistent with misexpression of insulin-like growth factor 2 (IGF2), an important facilitator of fetal growth. We propose that the IGF2-dependent BWS and SRS cases can be identified by prenatal diagnosis and can be prevented by prenatal intervention targeting IGF2. We test this hypothesis using our mouse models of IGF2-dependent BWS and SRS. We find that genetically normalizing IGF2 levels in a double rescue experiment corrects the fetal overgrowth phenotype in the BWS model and the growth retardation in the SRS model. In addition, we pharmacologically rescue the BWS growth phenotype by reducing IGF2 signaling during late gestation. This animal study encourages clinical investigations to target IGF2 for prenatal diagnosis and prenatal prevention in human BWS and SRS.
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