Cardiac fibrosis is a major public health issue characterized by fibroblast activation, abnormal proliferation, and excessive deposition of extracellular matrix (ECM) proteins. It is a complex process involving multiple mechanisms, with redox homeostasis playing a critical role in cardiac remodeling. Metal ion metabolism, including iron, copper, calcium, and zinc, is essential for maintaining redox balance and influencing cardiac fibrosis. Imbalances in metal ion homeostasis can lead to oxidative stress, which contributes to the development and progression of cardiac fibrosis. Iron metabolism is crucial for maintaining redox balance. Iron overload can lead to oxidative stress, which promotes fibroblast activation and cardiac fibrosis. Iron deficiency can also impair mitochondrial function and contribute to fibrosis. Ferroptosis, an iron-dependent form of cell death, is involved in the pathogenesis of cardiac fibrosis. Copper metabolism affects mitochondrial function and can lead to oxidative stress and cell death. Copper deficiency can impair mitochondrial respiration and contribute to cardiac fibrosis. Copper also mediates various forms of programmed cell death, including autophagy, apoptosis, pyroptosis, and cuproptosis. Calcium metabolism is essential for cardiac function and is closely linked to oxidative stress. Excess calcium can lead to oxidative stress and mitochondrial dysfunction, contributing to cardiac fibrosis. Calcium channels play a role in the regulation of oxidative stress and cardiac fibrosis. Zinc metabolism is also important for maintaining redox balance. Zinc deficiency can lead to oxidative stress and contribute to cardiac fibrosis. Metallothionein (MT), which helps scavenge reactive oxygen species (ROS), is affected by zinc metabolism. This review highlights the role of metal ion metabolism in cardiac fibrosis and the potential therapeutic interventions. The regulation of metal ion levels and their mediated redox processes is a promising target for the treatment of cardiac fibrosis. Further research is needed to fully understand the mechanisms and develop effective therapies.Cardiac fibrosis is a major public health issue characterized by fibroblast activation, abnormal proliferation, and excessive deposition of extracellular matrix (ECM) proteins. It is a complex process involving multiple mechanisms, with redox homeostasis playing a critical role in cardiac remodeling. Metal ion metabolism, including iron, copper, calcium, and zinc, is essential for maintaining redox balance and influencing cardiac fibrosis. Imbalances in metal ion homeostasis can lead to oxidative stress, which contributes to the development and progression of cardiac fibrosis. Iron metabolism is crucial for maintaining redox balance. Iron overload can lead to oxidative stress, which promotes fibroblast activation and cardiac fibrosis. Iron deficiency can also impair mitochondrial function and contribute to fibrosis. Ferroptosis, an iron-dependent form of cell death, is involved in the pathogenesis of cardiac fibrosis. Copper metabolism affects mitochondrial function and can lead to oxidative stress and cell death. Copper deficiency can impair mitochondrial respiration and contribute to cardiac fibrosis. Copper also mediates various forms of programmed cell death, including autophagy, apoptosis, pyroptosis, and cuproptosis. Calcium metabolism is essential for cardiac function and is closely linked to oxidative stress. Excess calcium can lead to oxidative stress and mitochondrial dysfunction, contributing to cardiac fibrosis. Calcium channels play a role in the regulation of oxidative stress and cardiac fibrosis. Zinc metabolism is also important for maintaining redox balance. Zinc deficiency can lead to oxidative stress and contribute to cardiac fibrosis. Metallothionein (MT), which helps scavenge reactive oxygen species (ROS), is affected by zinc metabolism. This review highlights the role of metal ion metabolism in cardiac fibrosis and the potential therapeutic interventions. The regulation of metal ion levels and their mediated redox processes is a promising target for the treatment of cardiac fibrosis. Further research is needed to fully understand the mechanisms and develop effective therapies.