Research Advances on Cadmium-Induced Toxicity in Hepatic Macrophages

Cadmium (Cd) is a highly toxic and pervasive environmental pollutant that exerts detrimental effects on human health through diverse biochemical and molecular mechanisms. As a vital metabolic organ, the liver harbors macrophages that play a crucial role in maintaining hepatic health and function. Current research has paid relatively little attention to the role of macrophages in liver injury induced by heavy metal exposure. This review summarizes current research on the molecular mechanisms underlying cadmium-induced toxicity in hepatic macrophages, focusing on oxidative stress, signaling pathways, gene transcription, and apoptosis. It further examines how cadmium-induced macrophage dysfunction impacts hepatic immunometabolism. Specifically, we detail how cadmium triggers oxidative stress and disrupts intracellular calcium homeostasis, leading to the activation of transcription factors such as <i>NF-κB</i> and <i>Nrf2</i>, and the subsequent engagement of related signaling cascades. These perturbations alter macrophage polarization (M1/M2), promote cellular damage and apoptosis, and ultimately exacerbate hepatic inflammation and fibrosis. By synthesizing recent advances in this field, this review aims to provide a theoretical foundation and future directions for research, with the goal of informing novel strategies for the prevention and treatment of heavy metal-associated liver diseases.