ArticleNeurotoxicity research2010
The role of zinc in the modulation of neuronal proliferation and apoptosis.
Article in Neurotoxicity research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 2 of them syntheses that pooled it.
What it found
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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
43 citing papers in PubMed, 2 syntheses or guidelines pooled it, 113 citations in OpenAlex.
- The Changes of Blood and CSF Ion Levels in Depressed Patients: a Systematic Review and Meta-analysis.Molecular neurobiology · 2024Pooled it
- Pooled it
- The role of zinc homeostasis in major depressive disorder: heterogeneous pathological mechanisms and therapeutic implications.Annals of medicine · 2026Review
- The therapeutic potential of zinc-nanoparticles against the cerebellar neurotoxicity induced by bacterial lipopolysaccharides in female rats and their pups.Scientific reports · 2026Article
- The Impact of Zinc on Cellular Dynamics, Brain Function, and its Therapeutic Potential in Neuronal Regeneration.Molecular neurobiology · 2026Review
- Magnesium and Zinc in Schizophrenia.Biomedicines · 2025Review
- Article
- Co-delivery of neurotrophic factors and a zinc chelator substantially increases retinal ganglion cell survival and axon protection in the optic nerve crush model.Acta biomaterialia · 2025Article
- Neural Stem Cell-based Regenerative Therapy: A New Approach to Diabetes Treatment.Endocrine, metabolic & immune disorders drug targets · 2024Review
- The Role of Glycogen Synthase Kinase-3β in the Zinc-Mediated Neuroprotective Effect of Metformin in Rats with Glutamate Neurotoxicity.Biological trace element research · 2024Article
- The role of zinc in the premature brain: functions, outcomes and future research perspectives.Frontiers in pediatrics · 2024Review
- Neurodevelopmental Consequences of Dietary Zinc Deficiency: A Status Report.Biological trace element research · 2023Review
- What Are the Functions of Zinc in the Nervous System?Neurology · 2023Article
- Article
- Zinc: From Biological Functions to Therapeutic Potential.International journal of molecular sciences · 2023Review
- The Important Role of Zinc in Neurological Diseases.Biomolecules · 2022Review
- Suitability of Banana and Plantain Fruits in Modulating Neurodegenerative Diseases: Implicating the In Vitro and In Vivo Evidence from Neuroactive Narratives of Constituent Biomolecules.Foods (Basel, Switzerland) · 2022Review
- Prenatal Zinc Deficient Mice as a Model for Autism Spectrum Disorders.International journal of molecular sciences · 2022Review
- The Role of Zinc in Axon Formation via the mTORC1 Pathway.Molecular neurobiology · 2022Article
- PTPRM Is Critical for Synapse Formation Regulated by Zinc Ion.Frontiers in molecular neuroscience · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Although a requirement of zinc (Zn) for normal brain development is well documented, the extent to which Zn can modulate neuronal proliferation and apoptosis is not clear. Thus, we investigated the role of Zn in the regulation of these two critical events. A low Zn availability leads to decreased cell viability in human neuroblastoma IMR-32 cells and primary cultures of rat cortical neurons. This occurs in part as a consequence of decreased cell proliferation and increased apoptotic cell death. In IMR-32 cells, Zn deficiency led to the inhibition of cell proliferation through the arrest of the cell cycle at the G0/G1 phase. Zn deficiency induced apoptosis in both proliferating and quiescent neuronal cells via the intrinsic apoptotic pathway. Reductions in cellular Zn triggered a translocation of the pro-apoptotic protein Bad to the mitochondria, cytochrome c release, and caspase-3 activation. Apoptosis is the resultant of the inhibition of the prosurvival extracellular-signal-regulated kinase, the inhibition of nuclear factor-kappa B, and associated decreased expression of antiapoptotic proteins, and to a direct activation of caspase-3. A deficit of Zn during critical developmental periods can have persistent effects on brain function secondary to a deregulation of neuronal proliferation and apoptosis.
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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.