Yang Bing, Wang Zhongyuan, Wang Shujuan, Li Xiaofeng
College of Animal Science, Anhui Science and Technology University, Fengyang, 233100, China.
Biol Trace Elem Res. 2025 Apr;203(4):2186-2205. doi: 10.1007/s12011-024-04307-0. Epub 2024 Jul 16.
Cadmium (Cd) is a highly toxic heavy metal that can cause severe liver damage in both humans and animals. However, the specific genes responsible for Cd-induced hepatotoxicity are still not fully understood. Therefore, the aim of this study was to identify the key genes associated with Cd-induced liver damage. To achieve this, we utilized the GSE19662 dataset from the Gene Expression Omnibus (GEO), which consisted of rat hepatocyte samples treated with cadmium chloride (CdCl) as well as control groups. By focusing on rat hepatocytes treated with 0.10 ppm of CdCl, the study identified 851 differentially expressed genes (DEGs), with 438 genes being upregulated and 413 genes being downregulated. Gene Ontology (GO) analysis revealed that these DEGs were primarily involved in inflammatory responses, xenobiotic metabolic processes, and the response to drugs and xenobiotic stimuli. Finally, the study identified several hub genes, including CYP2E1, CYP3A62, CYP2C11, CYP2C13, CYP2B3, HSP90B1, HSP90AA1, GSTA2, and MAPK8, which were associated with CdCl-induced liver damage. Furthermore, pathway analysis demonstrated that these hub genes were mainly linked to pathways involved in chemical carcinogenesis, metabolic processes, steroid hormone biosynthesis, retinol metabolism, linoleic acid metabolism, arachidonic acid metabolism, inflammatory mediator regulation, Ras, and protein processing in the endoplasmic reticulum. In conclusion, this study provides important insights into the molecular mechanisms underlying Cd-induced liver damage.
镉（Cd）是一种剧毒重金属，可在人类和动物体内造成严重的肝脏损伤。然而，导致镉诱导的肝毒性的具体基因仍未完全明确。因此，本研究的目的是确定与镉诱导的肝脏损伤相关的关键基因。为实现这一目标，我们利用了基因表达综合数据库（GEO）中的GSE19662数据集，该数据集由用氯化镉（CdCl）处理的大鼠肝细胞样本以及对照组组成。通过聚焦于用0.10 ppm CdCl处理的大鼠肝细胞，该研究确定了851个差异表达基因（DEG），其中438个基因上调，413个基因下调。基因本体论（GO）分析表明，这些DEG主要参与炎症反应、异源生物代谢过程以及对药物和异源生物刺激的反应。最后，该研究确定了几个枢纽基因，包括CYP2E1、CYP3A62、CYP2C11、CYP2C13、CYP2B3、HSP90B1、HSP90AA1、GSTA2和MAPK8，它们与CdCl诱导的肝脏损伤相关。此外，通路分析表明，这些枢纽基因主要与化学致癌、代谢过程、类固醇激素生物合成、视黄醇代谢、亚油酸代谢、花生四烯酸代谢、炎症介质调节、Ras以及内质网中的蛋白质加工等通路相关。总之，本研究为镉诱导的肝脏损伤的分子机制提供了重要见解。
