ArticleRedox biology2017
Zinc deficiency affects the STAT1/3 signaling pathways in part through redox-mediated mechanisms.
Article in Redox biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 39 citations in OpenAlex.
- Induction of aneuploidy by the metal-chelating agent neodecanoid acid in mammalian cells in vitro.Archives of toxicology · 2026Article
- Integration of Metabolic Pathways and Micronutrient Signals Influences Neurodevelopment by Modulating Neural Stem Cell Dynamics.Molecular neurobiology · 2026Review
- Pathophysiological significance of impaired KAT7-dependent histone H3K14 acetylation during zinc deficiency.Nature communications · 2026Article
- Zinc suppresses Stat3-driven IL-6 production in primary mouse adipocytes.Frontiers in immunology · 2026Article
- Sex-specific association between serum zinc concentration and incidence of abdominal obesity: A nine-year follow-up.Journal of diabetes and metabolic disorders · 2025Article
- Metal Ion Signaling in Biomedicine.Chemical reviews · 2025Review
- The role of redox-active iron, copper, manganese, and redox-inactive zinc in toxicity, oxidative stress, and human diseases.EXCLI journal · 2025Review
- Cellular zinc metabolism and zinc signaling: from biological functions to diseases and therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Regulation of anti-tumor immunity by metal ion in the tumor microenvironment.Frontiers in immunology · 2024Review
- Neurodevelopmental Consequences of Dietary Zinc Deficiency: A Status Report.Biological trace element research · 2023Review
- The Importance of Natural Antioxidants in Female Reproduction.Antioxidants (Basel, Switzerland) · 2023Review
- Zinc in Human Health and Infectious Diseases.Biomolecules · 2022Review
- Vitamin E and Metabolic Health: Relevance of Interactions with Other Micronutrients.Antioxidants (Basel, Switzerland) · 2022Review
- Review
- Soil zinc, serum zinc, and the potential for agronomic biofortification to reduce human zinc deficiency in Ethiopia.Scientific reports · 2021Article
- Zinc Modulates Several Transcription-Factor Regulated Pathways in Mouse Skeletal Muscle Cells.Molecules (Basel, Switzerland) · 2020Article
- Zinc deficiency induces abnormal development of the myocardium by promoting SENP5 overexpression.PloS one · 2020Article
- Soil Zinc Is Associated with Serum Zinc But Not with Linear Growth of Children in Ethiopia.Nutrients · 2019Article
- Zinc as a Gatekeeper of Immune Function.Nutrients · 2017Review
- Zinc Signals and Immunity.International journal of molecular sciences · 2017Review
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Zinc deficiency affects the development of the central nervous system (CNS) through mechanisms only partially understood. We previously showed that zinc deficiency causes CNS oxidative stress, damaging microtubules and impairing protein nuclear shuttling. STAT1 and STAT3 transcription factors, which require nuclear import for their functions, play major roles in CNS development. Thus, we investigated whether zinc deficiency disrupts STAT1 and STAT3 signaling pathways in the developing fetal CNS, characterizing the involvement of oxidative stress and the cytoskeleton in the adverse effects. Maternal (gestation day 0-19) marginal zinc deficiency (MZD) reduced STAT1 and STAT3 tyrosine phosphorylation and their nuclear translocation in the embryonic day 19 (E19) rat brain. Similar effects were observed in zinc depleted IMR-32 neuroblastoma cells, with an associated decrease in STAT1- and STAT3-dependent gene transactivation. Zinc deficiency caused oxidative stress (increased 4-hydroxynonenal-protein adducts) in E19 brain and IMR-32 cells, which was prevented in cells by supplementation with 0.5mM α-lipoic acid (LA). In zinc depleted IMR-32 cells, the low tyrosine phosphorylation of STAT1, but not that of STAT3, recovered upon incubation with LA. STAT1 and STAT3 nuclear transports were also restored by LA. Accordingly, chemical disruption of the cytoskeleton partially reduced STAT1 and STAT3 nuclear levels. In summary, the redox-dependent tyrosine phosphorylation, and oxidant-mediated disruption of the cytoskeleton are involved in the deleterious effects of zinc deficit on STAT1 and STAT3 activation and nuclear translocation. Therefore, disruption of the STAT1 and STAT3 signaling pathways may in part explain the deleterious effects of maternal MZD on fetal brain development.
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