ArticleToxicology2017
Cadmium impairs the survival and proliferation of cultured adult subventricular neural stem cells through activation of the JNK and p38 MAP kinases.
Article in Toxicology, 2017. 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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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.
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Who cites it
17 citing papers in PubMed, 60 citations in OpenAlex.
- The Effects of Lead, Cadmium and Arsenic Exposure Alone or in Combination on Neurotoxicity Through Neural Signaling Pathways.Biological trace element research · 2026Review
- From injury to recovery: transcriptomic dynamics in zebrafish brain regeneration.Journal of translational medicine · 2025Article
- Bisphenol-F and Bisphenol-S (BPF and BPS) Impair the Stemness of Neural Stem Cells and Neuronal Fate Decision in the Hippocampus Leading to Cognitive Dysfunctions.Molecular neurobiology · 2024Article
- Review
- Adult neurogenesis: a real hope or a delusion?Neural regeneration research · 2024Review
- Hybrid Nanoparticle/DNAzyme Electrochemical Biosensor for the Detection of Divalent Heavy Metal Ions and CrSensors (Basel, Switzerland) · 2023Article
- Kinase inhibit region of SOCS3 attenuates IL6-induced proliferation and astrocytic differentiation of neural stem cells via cross talk between signaling pathways.CNS neuroscience & therapeutics · 2023Article
- Heavy metals and adult neurogenesis.Current opinion in toxicology · 2021Article
- Cypermethrin Impairs Hippocampal Neurogenesis and Cognitive Functions by Altering Neural Fate Decisions in the Rat Brain.Molecular neurobiology · 2021Article
- Thyroid Stem Cells But Not Differentiated Thyrocytes Are Sensitive to Slightly Increased Concentrations of Heavy Metals.Frontiers in endocrinology · 2021Article
- Inducible and conditional activation of ERK5 MAP kinase rescues mice from cadmium-induced olfactory memory deficits.Neurotoxicology · 2020Article
- Inducible and Conditional Stimulation of Adult Hippocampal Neurogenesis Rescues Cadmium-Induced Impairments of Adult Hippocampal Neurogenesis and Hippocampus-Dependent Memory in Mice.Toxicological sciences : an official journal of the Society of Toxicology · 2020Article
- Cadmium Exposure Impairs Adult Hippocampal Neurogenesis.Toxicological sciences : an official journal of the Society of Toxicology · 2019Article
- Effects of environmental stressors on stem cells.World journal of stem cells · 2019Review
- MeHg-induced autophagy via JNK/Vps34 complex pathway promotes autophagosome accumulation and neuronal cell death.Cell death & disease · 2019Article
- Cadmium Exposure Impairs Cognition and Olfactory Memory in Male C57BL/6 Mice.Toxicological sciences : an official journal of the Society of Toxicology · 2018Article
- Identification of ARNT-regulated BIRC3 as the target factor in cadmium renal toxicity.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Cadmium (Cd) is a heavy metal with a long biological half-life in humans and is recognized as a toxic pollutant. Cd is also a potential neurotoxicant and its exposure is associated with olfactory impairment in humans. However, the molecular and cellular mechanisms of Cd neurotoxicity are not well defined. Adult neurogenesis is a process that generates functional neurons from adult neural stem/progenitor cells (aNPCs). It occurs in specific regions of the adult brain including the subventricular zone (SVZ) along the lateral ventricles in mammals, a process that is critical for olfaction. Various external stimuli can modulate adult neurogenesis and the effect of neurotoxicants on adult neurogenesis is just beginning to be elucidated. Since Cd exposure can impair olfaction in humans, the goal of this study is to investigate the effects of Cd on SVZ adult neurogenesis and underlying mechanisms using primary cultured SVZ-aNPCs. In this study, we report that low-level Cd exposure decreases cell number, induces apoptosis, and inhibits cell proliferation in SVZ-aNPCs. Furthermore, Cd exposure significantly increases phosphorylation of c-Jun NH2-terminal kinase (JNK), and p38 MAP kinase in these cells, indicative of JNK and p38 activation. Pharmacological inhibition of JNK or p38 MAPK kinases attenuated Cd-induced cell loss and apoptosis. Cd treatment did not cause cell loss or apoptosis in SVZ-aNPCs prepared from transgenic mice null for the neural-specific JNK3 isoform. These data suggest a critical role for p38 and JNK3 MAP kinases in Cd neurotoxicity. These results are, to our knowledge, the first demonstration that Cd impairs SVZ adult neurogenesis in vitro, which may contribute to its neurotoxicity in olfaction.
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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.