This review article explores the role of metal ion metabolism in cardiac fibrosis, focusing on iron, copper, calcium, and zinc. Cardiac fibrosis, characterized by excessive extracellular matrix (ECM) deposition and abnormal proliferation of fibroblasts, is a significant public health issue. The article highlights how imbalances in metal ion homeostasis can lead to redox dysregulation, contributing to the maladaptive process of cardiac fibrosis. Iron overload or deficiency, copper imbalance, calcium overload, and zinc deficiency are discussed in detail, each affecting mitochondrial function, oxidative stress, and redox homeostasis. Iron overload can cause oxidative stress and ferroptosis, while copper imbalance affects mitochondrial respiration and leads to various forms of cell death. Calcium overload impairs mitochondrial function and increases ROS production, and zinc deficiency reduces the clearance of ROS, leading to oxidative stress. The article also outlines potential therapeutic interventions and ongoing challenges in this field, emphasizing the need for further research to understand the exact mechanisms and develop effective treatments for cardiac fibrosis.This review article explores the role of metal ion metabolism in cardiac fibrosis, focusing on iron, copper, calcium, and zinc. Cardiac fibrosis, characterized by excessive extracellular matrix (ECM) deposition and abnormal proliferation of fibroblasts, is a significant public health issue. The article highlights how imbalances in metal ion homeostasis can lead to redox dysregulation, contributing to the maladaptive process of cardiac fibrosis. Iron overload or deficiency, copper imbalance, calcium overload, and zinc deficiency are discussed in detail, each affecting mitochondrial function, oxidative stress, and redox homeostasis. Iron overload can cause oxidative stress and ferroptosis, while copper imbalance affects mitochondrial respiration and leads to various forms of cell death. Calcium overload impairs mitochondrial function and increases ROS production, and zinc deficiency reduces the clearance of ROS, leading to oxidative stress. The article also outlines potential therapeutic interventions and ongoing challenges in this field, emphasizing the need for further research to understand the exact mechanisms and develop effective treatments for cardiac fibrosis.