Unveiling Cadmium-Induced Cardiotoxicity: Mechanisms, Challenges, and Future Perspectives: A Narrative Review

Abstract

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 longterm 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.