ArticlePloS one2011
Calcium signaling is involved in cadmium-induced neuronal apoptosis via induction of reactive oxygen species and activation of MAPK/mTOR network.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 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.
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Who cites it
99 citing papers in PubMed, 213 citations in OpenAlex.
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- Cd-IMAC-MS Enables Exploratory Profiling of Cadmium-Associated Proteins in Rat Brain after Cadmium Exposure.Biological trace element research · 2026Article
- BrCCX1 Negatively Regulates Calcium-Mediated Clubroot Resistance in Chinese Cabbage.Plant, cell & environment · 2026Article
- Cerebroprotective potential of ceftriaxone against cadmium chloride-induced cerebral inflammatory changes and oxidative insult.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Understanding the contribution of toxicant exposures to Alzheimer's disease and related dementias.Current opinion in neurobiology · 2026Review
- Review
- Agonism of MTNeurochemical research · 2025Article
- Environmental Toxins and Oxidative Stress: The Link to Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- Distinct In Vitro Differentiation Protocols Differentially Affect Cytotoxicity Induced by Heavy Metals in Human Neuroblastoma SH-SY5Y Cells.Biological trace element research · 2025Article
- Hippocampal Inhibitory Interneuron-Specific DREADDs Treatment Alters mTORC1-4E-BP Signaling and Impairs Memory Formation.Journal of neurochemistry · 2025Article
- Neurotoxic Effect of Myricitrin in Copper-Induced Oxidative Stress Is Mediated by Increased Intracellular CaAntioxidants (Basel, Switzerland) · 2025Article
- Zingerone Attenuates Cadmium-Induced Neuroinflammation, Oxidative Stress and Cognitive Deficit on the Prefrontal Cortex of Adult Wistar Rats.Journal of experimental pharmacology · 2025Article
- Molecular signature of cadmium-mediated neurodevelopmental disorders in prenatal to postnatal stages.EXCLI journal · 2025Review
- The Impact of Calcium Overload on Cellular Processes: Exploring Calcicoptosis and Its Therapeutic Potential in Cancer.International journal of molecular sciences · 2024Review
- Role of SIRT1 in Potentially Toxic Trace Elements (Lead, Fluoride, Aluminum and Cadmium) Associated Neurodevelopmental Toxicity.Biological trace element research · 2024Review
- One path, two solutions: Network-based analysis identifies targetable pathways for the treatment of comorbid type II diabetes and neuropsychiatric disorders.Computational and structural biotechnology journal · 2024Article
- Association of Urinary Cadmium Concentration With Cognitive Impairment in US Adults: A Longitudinal Cohort Study.Neurology · 2024Article
- Mechanisms of Phytoremediation by Resveratrol against Cadmium Toxicity.Antioxidants (Basel, Switzerland) · 2024Review
- Cadmium inhibits calcium activity in hippocampal CA1 neurons of freely moving mice.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- Early prediction of cognitive impairment in adults aged 20 years and older using machine learning and biomarkers of heavy metal exposure.Current research in toxicology · 2024Article
39 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Cadmium (Cd), a toxic environmental contaminant, induces oxidative stress, leading to neurodegenerative disorders. Recently we have demonstrated that Cd induces neuronal apoptosis in part by activation of the mitogen-activated protein kineses (MAPK) and mammalian target of rapamycin (mTOR) pathways. However, the underlying mechanism remains elusive. Here we show that Cd elevated intracellular calcium ion ([Ca²+](i)) level in PC12, SH-SY5Y cells and primary murine neurons. BAPTA/AM, an intracellular Ca²+ chelator, abolished Cd-induced [Ca²+](i) elevation, and blocked Cd activation of MAKPs including extracellular signal-regulated kinase 1/2 (Erk1/2), c-Jun N-terminal kinase (JNK) and p38, and mTOR-mediated signaling pathways, as well as cell death. Pretreatment with the extracellular Ca²+ chelator EGTA also prevented Cd-induced [Ca²+](i) elevation, MAPK/mTOR activation, as well as cell death, suggesting that Cd-induced extracellular Ca²+ influx plays a critical role in contributing to neuronal apoptosis. In addition, calmodulin (CaM) antagonist trifluoperazine (TFP) or silencing CaM attenuated the effects of Cd on MAPK/mTOR activation and cell death. Furthermore, Cd-induced [Ca²+](i) elevation or CaM activation resulted in induction of reactive oxygen species (ROS). Pretreatment with BAPTA/AM, EGTA or TFP attenuated Cd-induced ROS and cleavage of caspase-3 in the neuronal cells. Our findings indicate that Cd elevates [Ca²+](i), which induces ROS and activates MAPK and mTOR pathways, leading to neuronal apoptosis. The results suggest that regulation of Cd-disrupted [Ca²+](i) homeostasis may be a new strategy for prevention of Cd-induced neurodegenerative diseases.
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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 Socratic graph.