Related Experiment Video
Updated: May 2, 2026
Intracavernosal Pressure Recording to Evaluate Erectile Function in Rodents
Published on: June 6, 2018
Cadmium chloride and erectile dysfunction: integrative evidence from network toxicology, Mendelian randomization, and
Yuqi Li1, Qilong Wu1, Chunyang Meng1
1Department of Urology, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, China.
Background:
In recent years, heavy metal exposure has been increasingly implicated in the onset and progression of various diseases. However, the relationship between heavy metal exposure and male erectile function remains insufficiently understood. This study aimed to investigate the association between cadmium chloride (CdCl2) and erectile dysfunction (ED), and to explore the underlying molecular mechanisms.
Methods:
An integrated analytical framework was established to elucidate the potential link between cadmium chloride and ED. Key cadmium-ED related genes were first identified through comprehensive analyses using multiple databases, including PubChem, TargetNet, GeneCards, and STRING. Subsequently, Mendelian randomization (MR) analysis was conducted to assess the causal relationship between cadmium associated genes and ED. Finally, in vitro experiments were carried out to examine the effects of varying concentrations of CdCl2 on human umbilical vein endothelial cells (HUVECs), focusing on alterations in cell viability and gene expression.
Results:
Network toxicology analysis identified estrogen receptor 2 (ESR2) as a key gene mediating the link between cadmium chloride and ED. MR analysis demonstrated that increased ESR2 expression was causally associated with a higher risk of ED. In vitro experiments further showed that CdCl2 exposure led to a concentration- and time-dependent reduction in HUVEC viability, accompanied by upregulation of ESR2 expression.
Conclusion:
CdCl2 exposure may be associated with the onset and progression of erectile dysfunction, and its potential effects may involve multiple aspects, including vascular endothelial dysfunction, disruption of endocrine homeostasis, and abnormal ESR2 related signaling.
