ArticleJournal of neurochemistry2011
CaMKII is involved in cadmium activation of MAPK and mTOR pathways leading to neuronal cell death.
Article in Journal of neurochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 101 citations in OpenAlex.
- Understanding molecular mechanisms driving cadmium-induced mitochondrial dysfunction in human metabolic liver disease.Environmental toxicology and pharmacology · 2026Review
- Activity drives local CaMKII synthesis and subcellular localization via autophosphorylation-dependent pathways.bioRxiv : the preprint server for biology · 2025Article
- Automated gait analysis indicates efficacy of T-type calcium channel inhibition for mitigation of disrupted calcium signalling in an SCA5 mouse model.Scientific reports · 2025Article
- The Impact of Calcium Overload on Cellular Processes: Exploring Calcicoptosis and Its Therapeutic Potential in Cancer.International journal of molecular sciences · 2024Review
- A culture method with berbamine, a plant alkaloid, enhances CAR-T cell efficacy through modulating cellular metabolism.Communications biology · 2024Article
- Cadmium Exposure: Mechanisms and Pathways of Toxicity and Implications for Human Health.Toxics · 2024Review
- Environmental exposure of the general population to cadmium as a risk factor of the damage to the nervous system: A critical review of current data.Journal of applied toxicology : JAT · 2023Review
- Neuroprotection of resveratrol against cadmium-poisoning acts through dual inhibition of mTORC1/2 signaling.Neuropharmacology · 2022Article
- Disruption of brain conductivity and permittivity and neurotransmitters induced by citrate-coated silver nanoparticles in male rats.Environmental science and pollution research international · 2021Article
- Effects of myricetin against cadmium-induced neurotoxicity in PC12 cells.Toxicology research · 2021Article
- Epigenetic influence of environmentally neurotoxic metals.Neurotoxicology · 2020Review
- Rapamycin inhibits B-cell activating factor (BAFF)-stimulated cell proliferation and survival by suppressing CaCell calcium · 2020Article
- Dentin-Derived Inorganic Minerals Promote the Osteogenesis of Bone Marrow-Derived Mesenchymal Stem Cells: Potential Applications for Bone Regeneration.Stem cells international · 2020Article
- Heavy metal toxicity and the aetiology of glaucoma.Eye (London, England) · 2020Review
- Royal jelly mitigates cadmium-induced neuronal damage in mouse cortex.Molecular biology reports · 2019Article
- Trans-resveratrol Inhibits Tau Phosphorylation in the Brains of Control and Cadmium Chloride-Treated Rats by Activating PP2A and PI3K/Akt Induced-Inhibition of GSK3β.Neurochemical research · 2019Article
- BAFF inhibits autophagy promoting cell proliferation and survival by activating CaCellular signalling · 2019Article
- Modelling cadmium-induced cardiotoxicity using human pluripotent stem cell-derived cardiomyocytes.Journal of cellular and molecular medicine · 2018Article
- Activation of CaScientific reports · 2018Article
- Modeling cadmium-induced endothelial toxicity using human pluripotent stem cell-derived endothelial cells.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Cadmium (Cd), a toxic environmental contaminant, induces neurodegenerative diseases. Recently, we have shown that Cd elevates intracellular free calcium ion ([Ca(2+) ](i) ) level, leading to neuronal apoptosis partly by activating mitogen-activated protein kinases (MAPK) and mammalian target of rapamycin (mTOR) pathways. However, the underlying mechanism remains to be elucidated. In this study, we show that the effects of Cd-elevated [Ca(2+) ](i) on MAPK and mTOR network as well as neuronal cell death are through stimulating phosphorylation of calcium/calmodulin-dependent protein kinase II (CaMKII). This is supported by the findings that chelating intracellular Ca(2+) with 1,2-bis(o-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid tetra(acetoxymethyl) ester or preventing Cd-induced [Ca(2+) ](i) elevation using 2-aminoethoxydiphenyl borate blocked Cd activation of CaMKII. Inhibiting CaMKII with KN93 or silencing CaMKII attenuated Cd activation of MAPK/mTOR pathways and cell death. Furthermore, inhibitors of mTOR (rapamycin), c-Jun N-terminal kinase (SP600125) and extracellular signal-regulated kinase 1/2 (U0126), but not of p38 (PD169316), prevented Cd-induced neuronal cell death in part through inhibition of [Ca(2+) ](i) elevation and CaMKII phosphorylation. The results indicate that Cd activates MAPK/mTOR network triggering neuronal cell death, by stimulating CaMKII. Our findings underscore a central role of CaMKII in the neurotoxicology of Cd, and suggest that manipulation of intracellular Ca(2+) level or CaMKII activity may be exploited for prevention of Cd-induced neurodegenerative disorders.
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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.