ArticleBiological trace element research2021
Nephrotoxicity Profile of Cadmium Revealed by Proteomics in Mouse Kidney.
Article in Biological trace element research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed.
- mTOR-Mediated Autophagy Regulates Cadmium-Induced Kidney Injury via Pyroptosis.International journal of molecular sciences · 2025Article
- Involvement ofFrontiers in cell and developmental biology · 2025Review
- Testicular Toxicity in Rats Exposed to AlClBiological trace element research · 2024Article
- Rethinking Chronic Kidney Disease in the Aging Population.Life (Basel, Switzerland) · 2022Review
- Histomorphological and ultrastructural cadmium-induced kidney injuries and precancerous lesions in rats and screening for biomarkers.Bioscience reports · 2022Article
- ACSM3 suppresses the pathogenesis of high-grade serous ovarian carcinoma via promoting AMPK activity.Cellular oncology (Dordrecht, Netherlands) · 2022Article
- The function of omega-3 polyunsaturated fatty acids in response to cadmium exposure.Frontiers in immunology · 2022Review
- Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Cadmium (Cd) is a highly toxic metal and kidney is its main target. However, the molecular effects and associated potential impacts of Cd-accumulated kidney have not been well investigated. In this study, mouse was used as a model to investigate the Cd-induced proteomic profile change in kidney, and a total of 34 differentially expressed proteins were detected by two-dimensional gel electrophoresis (2-DE) and further identified by matrix-assisted laser desorption/ionization time of flight mass spectrometry (MALDI-TOF-MS). Through Gene Ontology analysis and KEGG pathway annotation, it showed that Cd-regulated kidney metabolism and promoted renal damage and cell migration. By validation of Western blotting and RT-qPCR, metastasis-related proteins LIM and SH3 domain protein 1 (LASP1) and phosphoenolpyruvate carboxykinase/cytosolic [GTP] (PEPCK1) were confirmed to be upregulated; Acyl-CoA synthetase medium-chain family member 3 (ACSM3) was downregulated. Furthermore, carcinoma development-related proteins initiation factor 4A (eIF4A) and pyridoxine-5'-phosphate oxidase (PNPO) were upregulated, and pyridoxal kinase (PK) was downregulated. The downregulation of Na(+)/H(+) exchange regulatory cofactor (NHERF3) might promote renal damage which associated with decrease of transferrin (TRF) in kidney. Taken together, our results revealed proteomic profile of Cd-induced nephrotoxicity and provided data for further insights into the mechanisms of Cd toxicity.
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Registered trials
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