Tehran University of Medical Sciences Iranian Journal of Public Health 2251-6085 54 8 2025 09 02 1678 1688 Mandana Pouladzadeh Emergency Medicine Department, Faculty of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran Masoud Danjeh Department of Cardiology, Shahid Beheshti University of Medical Sciences, Tehran, Iran Negin Yousefi Chermehini Emergency Medicine Department, Faculty of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran Somayeh Zamanifard Department of Cardiology, School of Medicine, Hajar Hospital, Shahrekord University of Medical Sciences, Shahrekord, Iran Ali Abesi Student Research Committee, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran Parisa Molaee Department of Cardiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran Hadi Rezaeeyan Asadabad School of Medical Sciences, Asadabad, Iran 2024 06 24 2025 04 23 We investigated the mechanisms of cadmium-induced cardiotoxicity, focusing on its pathophysiological effects, potential preventive strategies, and therapeutic interventions. We further explored approaches to mitigate long-term cardiovascular risks associated with cadmium exposure. This research analyzed the molecular and cellular pathways involved in cadmium toxicity, emphasizing oxidative stress, inflammation, endothelial dysfunction, platelet-leukocyte interactions, and cardiomyocyte damage. Experimental findings and existing literature were examined to uncover the mechanisms driving cadmium-induced cardiotoxicity and to identify potential therapeutic targets. Cadmium exposure leads to oxidative stress and inflammation, resulting in endothelial dysfunction, platelet-leukocyte activation, and thromboinflammation. It disrupts calcium signaling, elevates reactive oxygen species (ROS) production, and causes cardiomyocyte loss, ultimately impairing cardiac function. Cadmium also remodels ion channels and suppresses cardiomyocyte proliferation, intensifying its cardiotoxic effects. While current therapies focus on removing circulating cadmium, they do not address the residual cardiovascular damage caused by prior exposure. Cadmium exerts significant cardiotoxic effects through oxidative stress, inflammation, and cellular activation. Future therapeutic strategies should target these pathways, particularly the activation of platelets, leukocytes, and endothelial cells, to reduce cadmium-induced cardiovascular damage and improve long-term outcomes. https://ijph.tums.ac.ir/index.php/ijph/article/view/35885 https://ijph.tums.ac.ir/index.php/ijph/article/download/35885/8623