时间标签：数据日期 2026-10-31 · 生成时间 2026-11-01 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/10/28–2026/10/31 ｜ 情报发生日期 2026-10-31
研究问题
However, the associations between blood Cd levels and MASLD are subject to substantial confounding factors, including smoking, occupational exposure, and socioeconomic status, which limit epidemiological inference.；A deeper understanding of the hepatic responses to Cd under steatotic stress is important for developing a mechanistic model of how toxicological Cd challenges may aggravate steatotic liver injury.；This study aimed to characterize the hepatic responses to acute CdCl2 exposure in vitro and in vivo under steatotic conditions and to monitor previously implicated molecular pathways involved.
方法
Mice were randomly assigned to five groups (n = 6): Control, MASLD, CdCl2, MASLD+CdCl2, and MASLD+CdCl2+Rapamycin.；All procedures were approved by the Institutional Animal Care and Use Committee of Sun Yat-Sen University (SYSU-IACUC-2025-001246) and conducted in compliance with national guidelines for laboratory animal care and use.；Steatosis was validated by oil red O (ORO) staining, triglyceride (TG) quantification, and lipid droplet fluorescence imaging.；Briefly, debris was excluded based on forward scatter area (FSC-A) versus side scatter area (SSC-A), followed by singlet discrimination using FSC-H versus FSC-A.
核心结论
CdCl2 (4 μM) exposure alone had minimal effects on lipid accumulation, whereas cotreatment with CdCl2 significantly exacerbated FFA-induced lipid droplet fluorescence intensity and area (2.3-fold vs MASLD alone, P < 0.001).；CdCl2 also substantially reduced cell viability, with the most pronounced effect in FFA-treated cells (B; 45.3 ± 6.2% vs Control, P < 0.01; 32.7 ± 4.8% vs MASLD, P < 0.05), consistent with cytotoxicity and lipotoxicity.；Morphological changes, including cytoplasmic shrinkage, reduced adhesion, and floating cells, were most evident in the combined treatment group, consistent with viability data. ‖ 结论：Our results integrate cellular, animal, and molecular observations to develop a model of the mechanism by which acute Cd exposure may exacerbate hepatic injury under steatotic conditions; these findings should be interpreted within the context of short-term toxicological exposure models.
局限
Several limitations need to be recognized.；Future research should incorporate chronic environmentally relevant Cd exposure models and fully validated ICP-MS-based Cd quantification in both serum and liver tissue.；Our results integrate cellular, animal, and molecular observations to develop a model of the mechanism by which acute Cd exposure may exacerbate hepatic injury under steatotic conditions; these findings should be interpreted within the context of short-term toxicological exposure models.
对本项目的价值
★☆☆☆☆ 代谢轴既干预敏感性最高，也是老药新用供给最充足的来源。
全文来源
PMC JATS 全文（正文 32,258 字符，已过标题/DOI 逐字归属校验）
原文题录
- 英文标题：Cadmium Exposure Aggravates SREBP-1c-Mediated Hepatic Steatosis and Liver Injury in High-Fat Diet-Fed Mice.
- 期刊与标识：ACS Omega · PMID 42959881 · DOI 10.1021/acsomega.5c11799
B 级证据分级：B 级（同行评议临床前研究，主要为动物模型）
本文核心结论来自动物模型或体外细胞学，属临床前证据，不能外推至人体。「延长健康寿命」「改善功能」等表述在小鼠中的意义，与人类临床结局之间仍有距离。
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