ArticleBiological trace element research2023
JAK2/STAT3 Signaling Pathway and Klotho Gene in Cadmium-induced Neurotoxicity In Vitro and In Vivo.
Article in Biological trace element research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Cd-IMAC-MS Enables Exploratory Profiling of Cadmium-Associated Proteins in Rat Brain after Cadmium Exposure.Biological trace element research · 2026Article
- Protective Effects of Leonurine on Alcoholic Liver Injury Through Modulation of Oxidative Stress and JAK2-STAT3 Signaling.Current issues in molecular biology · 2026Article
- Klotho deficiency and cognitive impairment in dialysis patients: mechanisms, clinical evidence, and therapeutic implications.Frontiers in aging neuroscience · 2026Review
- The association between low-concentration heavy metal exposure and chronic kidney disease risk through α-klotho.Scientific reports · 2025Article
- Effect of Interaction of ATG7 and Plasma Metal Concentrations on Cognitive Impairment in Rural China.Journal of molecular neuroscience : MN · 2025Article
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Cadmium (Cd), a common heavy metal in the environment, is associated with cognitive impairment. In the present study, we carried out a preliminary inquiry to explore whether Cd causes neurotoxicity by regulating the JAK2/STAT3 signaling pathway and affecting the expression of klotho genes in vivo and in vitro, providing clues for the mechanism of Cd-induced cognitive dysfunction. The rat samples were injected with Cd chloride solution for 14 weeks, and the memory function of the rats was detected. Different concentrations of Cd and JAK2/STAT3 signaling pathway inhibitors were used to treat PC12 cells and thus detect the apoptosis rate. The protein expression levels of JAK2, p-JAK2, STAT3, p-STAT3, and klotho in rat and PC12 cell were detected by ELISA and Western blot, respectively. With the increase in exposure dose, the memory function of rats was severely impaired. The expression of p-JAK2 and p-STAT3 proteins was significantly up-regulated, whereas that of klotho was significantly down-regulated both in vivo and in vitro (p < 0.05). In comparison with the high-dose Cd exposure group, after adding tyrphostin AG490 (AG490), the apoptosis rate of PC12 cells increased, whereas the phosphorylation levels of JAK2 and STAT3 in the cells decreased significantly (p < 0.05). Cd exposure may cause neurotoxicity by regulating the JAK2/STAT3 signaling pathway and down-regulating klotho protein expression, leading to cognitive dysfunction.
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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.