ReviewFrontiers in cell and developmental biology2021
Diabetes, Oxidative Stress, and DNA Damage Modulate Cranial Neural Crest Cell Development and the Phenotype Variability of Craniofacial Disorders.
Review in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Craniofacial development: genetics, signaling pathways, teratogenic mechanisms, and clinal significance.Molecular biomedicine · 2026Review
- Functional Variants of the RAD51 Gene Contribute to Susceptibility to Non-Syndromic Orofacial Clefts in a Han Chinese Population.Orthodontics & craniofacial research · 2026Article
- Genetic and Molecular Characterization of Treacher Collins Syndrome in Three Mexican Families.International journal of molecular sciences · 2026Article
- Mathematical modeling predicts novel mechanisms of stream confinement from Trail/Colec12/Dan in the collective migration of cranial neural crest cells.Developmental dynamics : an official publication of the American Association of Anatomists · 2026Article
- Gene-environment interactions modulate the phenotype severity in mouse models of congenital craniofacial syndromes.The Journal of clinical investigation · 2025Article
- The Molecular Mechanism of Craniofacial Cartilage Deformity Induced by High Glucose in Zebrafish.Current issues in molecular biology · 2025Article
- Oxidative stress-mediated apoptosis via theFrontiers in pediatrics · 2025Article
- Untangling Zebrafish Genetic Annotation: Addressing Complexities and Nomenclature Issues in Orthologous Evaluation of TCOF1 and NOLC1.Journal of molecular evolution · 2024Article
- The transcription of the main gene associated with Treacher-Collins syndrome (TCOF1) is regulated by G-quadruplexes and cellular nucleic acid binding protein (CNBP).Scientific reports · 2024Article
- Dynamic enhancer landscapes in human craniofacial development.Nature communications · 2024Article
- Chronic paternal alcohol exposures induce dose-dependent changes in offspring craniofacial shape and symmetry.Frontiers in cell and developmental biology · 2024Article
- Frem1 activity is regulated by Sonic hedgehog signaling in the cranial neural crest mesenchyme during midfacial morphogenesis.Developmental dynamics : an official publication of the American Association of Anatomists · 2023Article
- RNA Polymerases I and III in development and disease.Seminars in cell & developmental biology · 2023Review
- Extracellular Vesicles and Membrane Protrusions in Developmental Signaling.Journal of developmental biology · 2022Review
- Embryonic Exposure to Cigarette Smoke Extract Impedes Skeletal Development and Evokes Craniofacial Defects in Zebrafish.International journal of molecular sciences · 2022Article
- The Role of Sonic Hedgehog in Human Holoprosencephaly and Short-Rib Polydactyly Syndromes.International journal of molecular sciences · 2021Review
- A Rare Incidence of Nonsyndromic Mandibular Incisor Agenesis in a Three-generation Family: Case Report and Literature Review.International journal of clinical pediatric dentistryArticle
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Craniofacial malformations are among the most common birth defects in humans and they often have significant detrimental functional, aesthetic, and social consequences. To date, more than 700 distinct craniofacial disorders have been described. However, the genetic, environmental, and developmental origins of most of these conditions remain to be determined. This gap in our knowledge is hampered in part by the tremendous phenotypic diversity evident in craniofacial syndromes but is also due to our limited understanding of the signals and mechanisms governing normal craniofacial development and variation. The principles of Mendelian inheritance have uncovered the etiology of relatively few complex craniofacial traits and consequently, the variability of craniofacial syndromes and phenotypes both within families and between families is often attributed to variable gene expression and incomplete penetrance. However, it is becoming increasingly apparent that phenotypic variation is often the result of combinatorial genetic and non-genetic factors. Major non-genetic factors include environmental effectors such as pregestational maternal diabetes, which is well-known to increase the risk of craniofacial birth defects. The hyperglycemia characteristic of diabetes causes oxidative stress which in turn can result in genotoxic stress, DNA damage, metabolic alterations, and subsequently perturbed embryogenesis. In this review we explore the importance of gene-environment associations involving diabetes, oxidative stress, and DNA damage during cranial neural crest cell development, which may underpin the phenotypic variability observed in specific craniofacial syndromes.
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